Relation Results

Identifier	Residue	Sequence	Organism
SIGNOR-279681	Ser10	NVRVSNGsPSLERMD	Homo sapiens
pmid	sentence
26146988	CDK5 knockdown in HEY cells significantly prolonged the half-life of TP53 and p27 Kip1 proteins (XREF_FIG).\|During neural stem cell differentiation, CDK5 can phosphorylate p27 at Thr187 and at Ser10, promoting neurite outgrowth as neurons differentiate .

Identifier	Residue	Sequence	Organism
SIGNOR-279680	Thr187	NAGSVEQtPKKPGLR	Homo sapiens
pmid	sentence
26146988	CDK5 knockdown in HEY cells significantly prolonged the half-life of TP53 and p27 Kip1 proteins (XREF_FIG).\|During neural stem cell differentiation, CDK5 can phosphorylate p27 at Thr187 and at Ser10, promoting neurite outgrowth as neurons differentiate [ xref ].

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence
SIGNOR-275544	Ser108	RPPTPKSsPQKTRKS
pmid	sentence
27346674	Vaccinia-related kinase 3 (VRK3), a member of the VRK family, is widely expressed in human tissues and increases VHR phosphatase activity through a direct binding\|Here we report that oxidative stress-induced cyclin-dependent kinase 5 (CDK5) activation stimulates neuroprotective signaling via phosphorylation of vaccinia-related kinase 3 (VRK3) at Ser 108. The binding of vaccinia H1-related (VHR) phosphatase to phosphorylated VRK3 increased its affinity for phospho-ERK and subsequently downregulated ERK activation\|

Publications:

1

Identifier	Residue	Sequence	Organism
SIGNOR-279451	Ser108	PPKYLKLsPKHPESN	Homo sapiens
pmid	sentence
30237421	These results confirm that CDK5 phosphorylates CLIC4 at serine 108.\|We found that activated CDK5 phosphorylated serine 108 in CLIC4, increasing CLIC4 protein stability, and accumulation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-278265	Ser1116	YRRRPPRsPDHKRYF	Homo sapiens
pmid	sentence
24607229	Cdk5 phosphorylates NR2B at Ser1116 and controls surface level expression.\|Reduction in Cdk5 activity, as well as disruption of Cdk5-NR2B interactions consistently increased NR2B surface levels and facilitated NMDA mediated synaptic function.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250663	Ser1123	RSRSRSRsPRPRGDS	Rattus norvegicus	Cerebral Cortical Neuron
pmid	sentence
12824184	We demonstrated that Cdk5 phosphorylated Ser-1176 in the neuregulin receptor ErbB2 and phosphorylated Thr-871 and Ser-1120 in the ErbB3 receptor. We identified the Ser-1120 sequence RSRSPR in ErbB3 as a novel phosphorylation consensus sequence of Cdk5. Finally, we found that Cdk5 activity is involved in neuregulin-induced Akt activity and neuregulin-mediated neuronal survival.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250664	Thr873	LLYSEAKtPIKWMAL	Rattus norvegicus	Cerebral Cortical Neuron
pmid	sentence
12824184	We demonstrated that Cdk5 phosphorylated Ser-1176 in the neuregulin receptor ErbB2 and phosphorylated Thr-871 and Ser-1120 in the ErbB3 receptor. We identified the Ser-1120 sequence RSRSPR in ErbB3 as a novel phosphorylation consensus sequence of Cdk5. Finally, we found that Cdk5 activity is involved in neuregulin-induced Akt activity and neuregulin-mediated neuronal survival.

Publications:

2

Organism:

Rattus Norvegicus

Identifier	Residue	Sequence	Organism
SIGNOR-278258	Ser1124	PPTSPQSsPRKGYTL	Homo sapiens
pmid	sentence
25189171	Our results demonstrate that the Cdk5-dependent activation of RapGEF2, spatial activation of Rap1 signalling and Rap1-facilitated surface localization of N-cadherin in the upper intermediate zone control neuronal migration and ultimately the architecture of the mammalian cerebral cortex.\|This demonstrates that Cdk5 phosphorylates RapGEF2 at Ser1124 in vitro .

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-164080	Ser114	RKLQGRPsPGPPAPE	Homo sapiens	Neuron
pmid	sentence
20213743	Together, our data suggest that cdk5 can phosphorylate enos at the ser-113 site and down-regulate enos-derived no levels.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-279685	Ser1147	S-->A	Homo sapiens
pmid	sentence
14704270	Cdk5 phosphorylation inhibited the inositol 5-phosphatase activity of synaptojanin 1, whereas dephosphorylation by calcineurin stimulated such activity.\|The activity of synaptojanin 1 was also stimulated by its interaction with endophilin 1, its major binding partner at the synapse. Notably, Cdk5 phosphorylated serine 1144, which is adjacent to the endophilin binding site.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-156836	Ser1179	LTNPPSLsPIRRKGK	Homo sapiens	Neuron
pmid	sentence
17611284	Huntingtin is an antiapoptotic proteinwe show here that huntingtin is phosphorylated by the cyclin-dependent kinase 5 (cdk5) at serines 1181 and 1201. Phosphorylation can be induced by dna damage in vitro and in vivo. The state of huntingtin phosphorylation is a crucial regulator of neuronal cell death. Absence of phosphorylation of huntingtin at serines 1181 and 1201 confers toxic properties to wild-type huntingtin in a p53-dependent manner in striatal neurons and accelerates neuronal death induced by dna damage.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-156840	Ser1199	EQASVPLsPKKGSEA	Homo sapiens	Neuron
pmid	sentence
17611284	Huntingtin is an antiapoptotic proteinwe show here that huntingtin is phosphorylated by the cyclin-dependent kinase 5 (cdk5) at serines 1181 and 1201. Phosphorylation can be induced by dna damage in vitro and in vivo. The state of huntingtin phosphorylation is a crucial regulator of neuronal cell death. Absence of phosphorylation of huntingtin at serines 1181 and 1201 confers toxic properties to wild-type huntingtin in a p53-dependent manner in striatal neurons and accelerates neuronal death induced by dna damage.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250666	Ser1232	SGHFTMRsPFKCDAC	Rattus norvegicus	Neuron
pmid	sentence
11675505	Here, we demonstrate that cyclin dependent kinase-5 (Cdk5) associates with and phosphorylates NR2A subunits at Ser-1232 in vitro and in intact cells. Moreover, we show that roscovitine, a selective Cdk5 inhibitor, blocks both long-term potentiation induction and NMDA-evoked currents in rat CA1 hippocampal neurons. These results suggest that Cdk5 plays a key role in synaptic transmission and plasticity through its up-regulation of NMDARs.

Publications:

1

Organism:

Rattus Norvegicus

Identifier	Residue	Sequence	Organism
SIGNOR-198111	Ser129	ICPSLPYsPVSSPQS	Homo sapiens
pmid	sentence
22778263	Cdk5 and gsk3 phosphorylate ser-129, ser-133, and ser-137. Mutation of ser-129, ser-133, and ser-137 increases autonomous activity with little change in ca2 /cam-dependent activity.

Identifier	Residue	Sequence	Organism
SIGNOR-198115	Ser133	LPYSPVSsPQSSPRL	Homo sapiens
pmid	sentence
22778263	Cdk5 and gsk3 phosphorylate ser-129, ser-133, and ser-137. Mutation of ser-129, ser-133, and ser-137 increases autonomous activity with little change in ca2 /cam-dependent activity.

Identifier	Residue	Sequence	Organism
SIGNOR-197945	Ser137	PVSSPQSsPRLPRRP	Homo sapiens
pmid	sentence
22778263	Cdk5 and gsk3 phosphorylate ser-129, ser-133, and ser-137. Mutation of ser-129, ser-133, and ser-137 increases autonomous activity with little change in ca2 /cam-dependent activity.

Publications:

3

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-170357	Ser13	ARKNAQPsPARAPAE	Homo sapiens	Leukemia Cell
pmid	sentence
21145489	We show that noxa is phosphorylated on a serine residue (s(13)) in the presence of glucose. Phosphorylation promotes its cytosolic sequestration and suppresses its apoptotic function. We identify cdk5 as the noxa kinase

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-153445	Ser131	HTDSRKDsPPAGSPA	Homo sapiens
pmid	sentence
17327227	Phosphorylation by cdk5 decreased the auto-ubiquitylation of parkin both in vitro and in vivo.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Brain

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-276168	Ser134	ARFAVAYsPARDAGN	Homo sapiens	HEK-293 Cell
pmid	sentence
18625302	In this study, we suggest that the phosphorylation and activation of PLD2 by cyclin-dependent kinase 5 (Cdk5) is critical for EGF-dependent insulin secretion. We determined that the phosphorylation site of PLD2 was located at Ser(134).

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-278395	Ser134	ARFAVAYsPARDAGN	Homo sapiens
pmid	sentence
18625302	In this study, we suggest that the phosphorylation and activation of PLD2 by cyclin-dependent kinase 5 (Cdk5) is critical for EGF-dependent insulin secretion.\|We determined that Cdk5 phosphorylates PLD2 at Ser 134 of PLD2 and that this phosphorylation was suggested to be important for EGF-dependent insulin secretion.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-279452	Ser142	NGLARLSsPVLHRLR	Homo sapiens
pmid	sentence
23979715	Phosphorylation of drebrin at S142 by Cdk5 relieves the intramolecular inhibition of F-actin bundling.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-195329	Ser1450	LQTSKYFsPPPPARS	Homo sapiens	Neuron
pmid	sentence
22220831	Here, we demonstrate that lmtk2 is phosphorylated on serine-1418 (lmtk2ser ) by cdk5/p35 and present evidence that this regulates its ability to phosphorylate pp1cthr __

Publications:

1

Organism:

Homo Sapiens

Tissue:

Brain

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-156414	Ser15	PSVEPPLsQETFSDL	Homo sapiens	Neuron
pmid	sentence
17591690	Here, we demonstrate for the first time that cdk5 interacts with p53 and increases its stability through posttranslational regulation, leading to accumulation of p53, particularly in the nucleus. We show that cdk5 phosphorylates p53 on ser15, ser33 and ser46 in vitro,

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-156418	Ser20	PLSQETFsDLWKLLP	Homo sapiens	Neuron
pmid	sentence
17591690	Here, we demonstrate for the first time that cdk5 interacts with p53 and increases its stability through posttranslational regulation, leading to accumulation of p53, particularly in the nucleus. We show that cdk5 phosphorylates p53 on ser15, ser33 and ser46 in vitro,

Identifier	Residue	Sequence	Organism
SIGNOR-156422	Ser33	LPENNVLsPLPSQAM	Homo sapiens
pmid	sentence
17591690	We show that cdk5 phosphorylates p53 on ser15, ser33 and ser46 cdk5-stabilized p53 protein is transcriptionally active

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-156426	Ser46	AMDDLMLsPDDIEQW	Homo sapiens	Neuron
pmid	sentence
17591690	We show that cdk5 phosphorylates p53 on ser15, ser33 and ser46 cdk5-stabilized p53 protein is transcriptionally active

Publications:

4

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-173685	Ser154	AKPEPSPsPRITRKS	Homo sapiens
pmid	sentence
21565170	We report that cyclin-dependent kinases (cdks) 1, 2 and 5 can phosphorylate ser154 of human dnmt1 in vitro. Further evidence of phosphorylation of endogenous dnmt1 at position 154 by cdks is also found in 293 cells treated with roscovitine, a specific inhibitor of cdk1, 2 and 5

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-275966	Ser159	GIPVRCYsAEVVTLW	in vitro
pmid	sentence
10500146	We also show that casein kinase I, but not casein kinase II, can phosphorylate and activate cdk5 in vitro. Ser(159) in cdk5 is homologous to the regulatory Thr(160) in cdk2.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-250798	Ser159	GIPVRCYsAEVVTLW	in vitro
pmid	sentence
10500146	We also show that casein kinase I, but not casein kinase II, can phosphorylate and activate cdk5 in vitro.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-278923	Ser159	GIPVRCYsAEVVTLW	Homo sapiens
pmid	sentence
14586172	In addition, the Cdk7 substrate, CTD of RNAPII, causes a dose-dependent decline in Cdk5 activation by Cdk7.\|Likewise, Cdk7 or cyclin H immunoprecipitate from mouse brain specifically phosphorylates wt Cdk5 at Ser159 and enhances Cdk5 and p25 activity.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-262931	Ser160	GVTKAISsPTVSRLT	in vitro
pmid	sentence
17693641	Here we show that TPPP induces tubulin self-assembly into intact frequently bundled microtubules, and that the phosphorylation of specific sites distinctly affects the function of TPPP. The phosphorylation sites Thr(14), Ser(18), Ser(160) for Cdk5; Ser(18), Ser(160) for ERK2, and Ser(32) for PKA were identified by mass spectrometry. The phosphorylation by ERK2 or Cdk5 resulted in the loss of microtubule-assembling activity of TPPP.

Identifier	Residue	Sequence	Organism
SIGNOR-262932	Ser18	ANRTPPKsPGDPSKD	in vitro
pmid	sentence
17693641	Here we show that TPPP induces tubulin self-assembly into intact frequently bundled microtubules, and that the phosphorylation of specific sites distinctly affects the function of TPPP. The phosphorylation sites Thr(14), Ser(18), Ser(160) for Cdk5; Ser(18), Ser(160) for ERK2, and Ser(32) for PKA were identified by mass spectrometry. The phosphorylation by ERK2 or Cdk5 resulted in the loss of microtubule-assembling activity of TPPP.

Identifier	Residue	Sequence	Organism
SIGNOR-262933	Thr14	PAKAANRtPPKSPGD	in vitro
pmid	sentence
17693641	Here we show that TPPP induces tubulin self-assembly into intact frequently bundled microtubules, and that the phosphorylation of specific sites distinctly affects the function of TPPP. The phosphorylation sites Thr(14), Ser(18), Ser(160) for Cdk5; Ser(18), Ser(160) for ERK2, and Ser(32) for PKA were identified by mass spectrometry. The phosphorylation by ERK2 or Cdk5 resulted in the loss of microtubule-assembling activity of TPPP.

Publications:

3

Organism:

In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-279453	Ser17	GGPLRSAsPHRSAYE	Homo sapiens
pmid	sentence
29786422	CDK5 decreased the expression of both spinophilin (30%) and neurabin (64%).\|This suggests that CDK5 phosphorylation of spinophilin at Ser17 is not responsible for the CDK5 dependent increase in the spinophilin and PP1 association.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-279515	Ser191	SRHAIMRsPQMVSAI	Homo sapiens
pmid	sentence
26509276	By combining multiple network relations with PTM proteoform specific functional information, we proposed a mechanism to explain the observation that the cyclin dependent kinase CDK5 positively regulates beta-catenin co-activator activity.\|CDK5 phosphorylates beta-catenin on Ser-191 and Ser-246 (PR:000037229)

Identifier	Residue	Sequence	Organism
SIGNOR-279516	Ser246	ALVKMLGsPVDSVLF	Homo sapiens
pmid	sentence
26509276	By combining multiple network relations with PTM proteoform specific functional information, we proposed a mechanism to explain the observation that the cyclin dependent kinase CDK5 positively regulates beta-catenin co-activator activity.\|CDK5 phosphorylates beta-catenin on Ser 191 and Ser 246 (PR :000037229)

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250675	Ser198	TRKSAPSsPTLDCEK	Mus musculus	Brain
pmid	sentence
12796778	Three specific phosphorylation sites (Ser198, Thr219 and Ser231) and two weak phosphorylation sites (Ser242 and Thr245) for CDK5/p35 are located in this region of NUDEL \| Each single or double mutant compromised,and the triple mutant completely eliminated, interaction with 14-3-3ε. \| 14-3-3ε sustains NUDEL phosphorylation and protects it from phosphatase.e dynein motor function.

Identifier	Residue	Sequence	Organism
SIGNOR-250676	Ser231	GTENTFPsPKAIPNG	Mus musculus
pmid	sentence
12796778	Three specific phosphorylation sites (Ser198, Thr219 and Ser231) and two weak phosphorylation sites (Ser242 and Thr245) for CDK5/p35 are located in this region of NUDEL \| Each single or double mutant compromised,and the triple mutant completely eliminated, interaction with 14-3-3ε. \| 14-3-3ε sustains NUDEL phosphorylation and protects it from phosphatase.e dynein motor function.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250677	Ser242	IPNGFGTsPLTPSAR	Mus musculus	Brain
pmid	sentence
12796778	Three specific phosphorylation sites (Ser198, Thr219 and Ser231) and two weak phosphorylation sites (Ser242 and Thr245) for CDK5/p35 are located in this region of NUDEL \| Each single or double mutant compromised,and the triple mutant completely eliminated, interaction with 14-3-3ε. \| 14-3-3ε sustains NUDEL phosphorylation and protects it from phosphatase.e dynein motor function.

Publications:

3

Organism:

Mus Musculus

Identifier	Residue	Sequence	Organism
SIGNOR-154401	Ser203	DLEFSSGsPGKETNE	Homo sapiens
pmid	sentence
17440046	Cdk5 phosphorylated gr at multiple serines, including ser203 and ser211 of its n-terminal domain, and suppressed the transcriptional activity of this receptor on glucocorticoid-responsive promoters by attenuating attraction of transcriptional cofactors to dna.\| the effect of CDK5 on GR-induced transcriptional activity is specific to gene promoter, and possibly, to tissue

Identifier	Residue	Sequence	Organism
SIGNOR-154405	Ser211	PGKETNEsPWRSDLL	Homo sapiens
pmid	sentence
17440046	Cdk5 phosphorylated gr at multiple serines, including ser203 and ser211 of its n-terminal domain, and suppressed the transcriptional activity of this receptor on glucocorticoid-responsive promoters by attenuating attraction of transcriptional cofactors to dna.\| the effect of CDK5 on GR-induced transcriptional activity is specific to gene promoter, and possibly, to tissue

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-171018	Ser235	SPQDSPPsKASPAQD	Homo sapiens
pmid	sentence
21215781	Cdk5 regulates app (amyloid precursor protein) processing and tau hyperphosphorylationtau phosphorylation at t231, s235 and s262 also contributes to the dissociation of tau from microtubules

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-92603	Ser519	SGYSSPGsPGTPGSR	Homo sapiens	Alzheimer Disease Specific Cell Type
pmid	sentence
12226093	Phosphopeptide mapping revealed enhanced phosphorylation of ser(202)/thr(205) residues by p25-cdk5 considering the fact that phosphorylation of ser(202)/thr(205) antagonizes the tau-mediated nucleation of tubulin, p25-cdk5 may play a pivotal role in neuronal cell death in alzheimer's disease.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-92607	Thr522	SSPGSPGtPGSRSRT	Homo sapiens	Alzheimer Disease Specific Cell Type
pmid	sentence
12226093	Phosphopeptide mapping revealed enhanced phosphorylation of ser(202)/thr(205) residues by p25-cdk5 considering the fact that phosphorylation of ser(202)/thr(205) antagonizes the tau-mediated nucleation of tubulin, p25-cdk5 may play a pivotal role in neuronal cell death in alzheimer's disease.

Identifier	Residue	Sequence	Organism
SIGNOR-171022	Thr548	KKVAVVRtPPKSPSS	Homo sapiens
pmid	sentence
21215781	However, other kinases, such as cdk5, p38 and pka, also phosphorylate tau at t231tau phosphorylation at t231, s235 and s262 also contributes to the dissociation of tau from microtubules

Publications:

4

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-279150	Ser25	DTPPLEHsPAHLPNQ	Homo sapiens
pmid	sentence
28502042	Cdk5 was shown to phosphorylate PSD-95 at three sites, Thr19, Ser25, and Ser35, in PSD fractions, which reduces the ability of PSD-95 to multimerize, resulting in decreased NMDAR clustering (Table 2).

Identifier	Residue	Sequence	Organism
SIGNOR-279151	Ser35	HLPNQANsPPVIVNT	Homo sapiens
pmid	sentence
28502042	Cdk5 was shown to phosphorylate PSD-95 at three sites, Thr19, Ser25, and Ser35, in PSD fractions, which reduces the ability of PSD-95 to multimerize, resulting in decreased NMDAR clustering (Table 2).

Identifier	Residue	Sequence	Organism
SIGNOR-279152	Thr19	YRYQDEDtPPLEHSP	Homo sapiens
pmid	sentence
28502042	Cdk5 was shown to phosphorylate PSD-95 at three sites, Thr19, Ser25, and Ser35, in PSD fractions, which reduces the ability of PSD-95 to multimerize, resulting in decreased NMDAR clustering (Table 2).

Publications:

3

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-250648	Ser272	EEPSPLPsPTASPNH	in vitro
pmid	sentence
11113134	Amphiphysin is phosphorylated by cdk5 in a region including serines 272, 276, and 285. Amphiphysin 1 is also phosphorylated by the cdc2/cyclin B kinase complex in the same region and undergoes mitotic phosphorylation in dividing cells.

Identifier	Residue	Sequence	Organism
SIGNOR-250649	Ser276	PLPSPTAsPNHTLAP	in vitro
pmid	sentence
11113134	Amphiphysin is phosphorylated by cdk5 in a region including serines 272, 276, and 285. Amphiphysin 1 is also phosphorylated by the cdc2/cyclin B kinase complex in the same region and undergoes mitotic phosphorylation in dividing cells.

Identifier	Residue	Sequence	Organism
SIGNOR-250650	Ser285	NHTLAPAsPAPARPR	in vitro
pmid	sentence
11113134	Amphiphysin is phosphorylated by cdk5 in a region including serines 272, 276, and 285. Amphiphysin 1 is also phosphorylated by the cdc2/cyclin B kinase complex in the same region and undergoes mitotic phosphorylation in dividing cells.

Publications:

3

Organism:

In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-278189	Ser273	TGKTTDKsPFVIYDM	Homo sapiens
pmid	sentence
25827822	CDK5 in turn phosphorylates PPARgamma at Ser273 and prevents the transcription of specific PPARgamma target genes that have anti-diabetic effects .

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-279399	Ser274	TLELGGKsPCIVLAD	Homo sapiens
pmid	sentence
29948941	Cdk5 Phosphorylates ALDH1A1 at S75 and S274.\|These results demonstrate that Cdk5 increases ALDH1A1 levels in neurotoxin exposed neuronal cells both at transcriptional level and by direct phosphorylation at S75 and S274 sites.

Identifier	Residue	Sequence	Organism
SIGNOR-279400	Ser75	RQAFQIGsPWRTMDA	Homo sapiens
pmid	sentence
29948941	Cdk5 Phosphorylates ALDH1A1 at S75 and S274.\|These results demonstrate that Cdk5 increases ALDH1A1 levels in neurotoxin exposed neuronal cells both at transcriptional level and by direct phosphorylation at S75 and S274 sites.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-178660	Ser279	KSKTLDNsDLHPGPP	Homo sapiens	Neuron, Glioblastoma Cell
pmid	sentence
18487454	Here, we demonstrate that cyclin dependent kinase 5 (cdk5), a protein known to function mainly in postmitotic neurons, directly phosphorylates pike-a at ser-279 in its gtpase domain in glioblastoma cells. This phosphorylation event stimulates pike-a gtpase activity and the activity of its downstream effector akt.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-277502	Ser291	STPLHSPsPIRVHTV	Homo sapiens	HEK-293T Cell
pmid	sentence
31955914	CDK5-mediated phosphorylation on S297 promotes BAG3 degradation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence
SIGNOR-272929	Ser308	LIPKMKIsPKRMSCS
pmid	sentence
31488827	Here, we identify TRIM59 as a substrate of CDK5. EGFR-activated CDK5 directly binds to and phosphorylates TRIM59, a ubiquitin ligase at serine 308, which recruits PIN1 for cis-trans isomerization of TRIM59, leading to TRIM59 binding to importin α5 and nuclear translocation.

Publications:

1

Identifier	Residue	Sequence	Organism
SIGNOR-112418	Ser313	RCRTLSGsPRPKNFK	Chlorocebus aethiops
pmid	sentence
11733001	P70ik3-1 is phosphorylated by either cyclin A/cdk3 or cyclin E/cdk3 reconstituted in COS7 cells. Accordingly, we can conclude that in COS7 cells, Ser274 in p70ik3-1 is phosphorylated by endogenous kinases other than cdk5 (Fig. 4), at least one of which is cdk3 as shown in this work. Currently, however, the question of how ik3-1 function is modified by its cdk3-mediated phosphorylation of Ser274 remains to be adressed.

Publications:

1

Organism:

Chlorocebus Aethiops

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-273607	Ser318	QGRESKGsPKKRLDV	Rattus norvegicus	Neuron
pmid	sentence
21487013	We show that scapinin is phosphorylated at a highly conserved site in the central region of the protein (Ser-277) by Cdk5 in vitro. Expression of a scapinin phospho-mimetic mutant (S277D) restored normal axon elongation without affecting actin binding. Instead, phosphorylated scapinin was sequestered in the cytoplasm of neurons and away from the axon.

Publications:

1

Organism:

Rattus Norvegicus

Identifier	Residue	Sequence	Organism
SIGNOR-259401	Ser321	GLHSTPDsPAKPEKN	Homo sapiens
pmid	sentence
24391960	These results indicate that Cdk5-mediated phosphorylation of S321 inhibits DRD2 function, providing a novel regulatory mechanism for dopamine signaling.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Dopaminergic Synapse

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-264407	Ser350	ERQASLAsPSLRTSH	Mus musculus	NG-108-15 Cell
pmid	sentence
32047117	Cdk5 phosphorylates the 5-HT6R on serine 350 (Ser350)\|This suggests that the 5-HT6R is unable to interact with GPRIN1 when it is phosphorylated by Cdk5.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Sequence	Organism
SIGNOR-279684	Ser368	PNPSTSAsPKKSPPP	Homo sapiens
pmid	sentence
35443760	Cdk5 phosphorylation-induced SIRT2 nuclear translocation promotes the death of dopaminergic neurons in Parkinson's disease.\|Moreover, the cyclin-dependent kinase 5 (Cdk5)-mediated phosphorylation of SIRT2 at the Ser331 and Ser335 sites appears to be necessary for such nuclear translocation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-166682	Ser38	SVPEFPLsPPKKKDL	Homo sapiens
pmid	sentence
20630875	Involved in the regulation of the microtubule (mt) filament system by destabilizing microtubules. Prevents assembly and promotes disassembly of microtubules. The kinases involved in phosphorylating stmn ser-16 and ser-63 include camp-dependent protein kinase (pka) and pak1, whereas stmn ser-25 and ser-38 have been shown to be targets for proline-directed serine/threonine kinases such as cyclin-dependent kinases, erk1/2, and members of the p38 mapk subfamily.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-174598	Ser400	IHKVILGsPAHRAGL	Homo sapiens
pmid	sentence
21701498	Here we report that cyclin-dependent kinase-5 (cdk5), a kinase implicated in the pathogenesis of several neurodegenerative diseases, is responsible for phosphorylating htra2 at s400.We have shown previously that phosphomimetic mutants of htra2 at s400 result in increased proteolytic activity and contribute to enhanced resistance to mitochondrial stress

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-100574	Ser408	SIKSEPIsPPRDRMT	Homo sapiens	Cerebral Cortical Neuron
pmid	sentence
12691662	Cdk5-mediated inhibition of the protective effects of transcription factor mef2 in neurotoxicity-induced apoptosis.We have identified the prosurvival transcription factor mef2 as a direct nuclear target of cdk5. Cdk5 phosphorylates mef2 at a distinct serine in its transactivation domain to inhibit mef2 activity.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-185210	Ser425	TMLEDSVsPKKSTVL	Homo sapiens
pmid	sentence
19363486	Cdk5 phosphorylated talin head at ser 425, inhibiting its binding to smurf1, thus preventing talin head ubiquitylation and degradation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-279509	Ser444	SIKSEPVsPSRERSP	Homo sapiens
pmid	sentence
19812325	In this case, cdk5 phosphorylates MEF2D on Ser444 suppressing its transcriptional activity.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-265100	Ser486	LPITVPKsPAFALKN	Homo sapiens
pmid	sentence
31272499	CDK5-mediated phosphorylation and stabilization of TPX2 promotes hepatocellular tumorigenesis

Publications:

1

Organism:

Homo Sapiens

Tissue:

Hepatobiliary Carcinoma Cell

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-249327	Ser516	GDRSGYSsPGSPGTP	Homo sapiens	Alzheimer Disease Specific Cell Type
pmid	sentence
12387894	We found that cdk5 phosphorylated tau(441) at Thr-181, Ser-199, Ser-202, Thr-205, Thr-212, Ser-214, Thr-217, Thr-231, Ser-235, Ser-396, and Ser-404, but not at Ser-262, Ser-400, Thr-403, Ser-409, Ser-413, or Ser-422. GSK-3beta phosphorylated all the cdk5-catalyzed sites above except Ser-235.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-249317	Ser519	SGYSSPGsPGTPGSR	Homo sapiens	Alzheimer Disease Specific Cell Type
pmid	sentence
12387894	We found that cdk5 phosphorylated tau(441) at Thr-181, Ser-199, Ser-202, Thr-205, Thr-212, Ser-214, Thr-217, Thr-231, Ser-235, Ser-396, and Ser-404, but not at Ser-262, Ser-400, Thr-403, Ser-409, Ser-413, or Ser-422. GSK-3beta phosphorylated all the cdk5-catalyzed sites above except Ser-235.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-249318	Ser531	GSRSRTPsLPTPPTR	Homo sapiens	Alzheimer Disease Specific Cell Type
pmid	sentence
12387894	We found that cdk5 phosphorylated tau(441) at Thr-181, Ser-199, Ser-202, Thr-205, Thr-212, Ser-214, Thr-217, Thr-231, Ser-235, Ser-396, and Ser-404, but not at Ser-262, Ser-400, Thr-403, Ser-409, Ser-413, or Ser-422. GSK-3beta phosphorylated all the cdk5-catalyzed sites above except Ser-235.

Identifier	Residue	Sequence	Organism
SIGNOR-249319	Ser552	VVRTPPKsPSSAKSR	Homo sapiens
pmid	sentence
12387894	We found that cdk5 phosphorylated tau(441) at Thr-181, Ser-199, Ser-202, Thr-205, Thr-212, Ser-214, Thr-217, Thr-231, Ser-235, Ser-396, and Ser-404, but not at Ser-262, Ser-400, Thr-403, Ser-409, Ser-413, or Ser-422. GSK-3beta phosphorylated all the cdk5-catalyzed sites above except Ser-235.

Identifier	Residue	Sequence	Organism
SIGNOR-249320	Ser713	GAEIVYKsPVVSGDT	Homo sapiens
pmid	sentence
12387894	We found that cdk5 phosphorylated tau(441) at Thr-181, Ser-199, Ser-202, Thr-205, Thr-212, Ser-214, Thr-217, Thr-231, Ser-235, Ser-396, and Ser-404, but not at Ser-262, Ser-400, Thr-403, Ser-409, Ser-413, or Ser-422. GSK-3beta phosphorylated all the cdk5-catalyzed sites above except Ser-235.

Identifier	Residue	Sequence	Organism
SIGNOR-249321	Ser721	PVVSGDTsPRHLSNV	Homo sapiens
pmid	sentence
12387894	We found that cdk5 phosphorylated tau(441) at Thr-181, Ser-199, Ser-202, Thr-205, Thr-212, Ser-214, Thr-217, Thr-231, Ser-235, Ser-396, and Ser-404, but not at Ser-262, Ser-400, Thr-403, Ser-409, Ser-413, or Ser-422. GSK-3beta phosphorylated all the cdk5-catalyzed sites above except Ser-235.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-249326	Thr498	KTPPAPKtPPSSGEP	Homo sapiens	Alzheimer Disease Specific Cell Type
pmid	sentence
12387894	We found that cdk5 phosphorylated tau(441) at Thr-181, Ser-199, Ser-202, Thr-205, Thr-212, Ser-214, Thr-217, Thr-231, Ser-235, Ser-396, and Ser-404, but not at Ser-262, Ser-400, Thr-403, Ser-409, Ser-413, or Ser-422. GSK-3beta phosphorylated all the cdk5-catalyzed sites above except Ser-235.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-249322	Thr522	SSPGSPGtPGSRSRT	Homo sapiens	Alzheimer Disease Specific Cell Type
pmid	sentence
12387894	We found that cdk5 phosphorylated tau(441) at Thr-181, Ser-199, Ser-202, Thr-205, Thr-212, Ser-214, Thr-217, Thr-231, Ser-235, Ser-396, and Ser-404, but not at Ser-262, Ser-400, Thr-403, Ser-409, Ser-413, or Ser-422. GSK-3beta phosphorylated all the cdk5-catalyzed sites above except Ser-235.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-249323	Thr529	TPGSRSRtPSLPTPP	Homo sapiens	Alzheimer Disease Specific Cell Type
pmid	sentence
12387894	We found that cdk5 phosphorylated tau(441) at Thr-181, Ser-199, Ser-202, Thr-205, Thr-212, Ser-214, Thr-217, Thr-231, Ser-235, Ser-396, and Ser-404, but not at Ser-262, Ser-400, Thr-403, Ser-409, Ser-413, or Ser-422. GSK-3beta phosphorylated all the cdk5-catalyzed sites above except Ser-235.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-249324	Thr534	SRTPSLPtPPTREPK	Homo sapiens	Alzheimer Disease Specific Cell Type
pmid	sentence
12387894	We found that cdk5 phosphorylated tau(441) at Thr-181, Ser-199, Ser-202, Thr-205, Thr-212, Ser-214, Thr-217, Thr-231, Ser-235, Ser-396, and Ser-404, but not at Ser-262, Ser-400, Thr-403, Ser-409, Ser-413, or Ser-422. GSK-3beta phosphorylated all the cdk5-catalyzed sites above except Ser-235.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-249325	Thr548	KKVAVVRtPPKSPSS	Homo sapiens	Alzheimer Disease Specific Cell Type
pmid	sentence
12387894	We found that cdk5 phosphorylated tau(441) at Thr-181, Ser-199, Ser-202, Thr-205, Thr-212, Ser-214, Thr-217, Thr-231, Ser-235, Ser-396, and Ser-404, but not at Ser-262, Ser-400, Thr-403, Ser-409, Ser-413, or Ser-422. GSK-3beta phosphorylated all the cdk5-catalyzed sites above except Ser-235.

Publications:

11

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-277356	Ser516	SIRPALNsPVERPSS	Homo sapiens	HEK-293 Cell
pmid	sentence
28528366	We found that GP78 expression is decreased in MPTP-based cellular and animal PD models, and CDK5 directly phosphorylated GP78 at Ser516, which promoted the ubiquitination and degradation of GP78.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-145963	Ser518	KGGTPAGsARGSPTR	Homo sapiens
pmid	sentence
16611631	Together, these results suggest that crmp4 is able to increase neurite formation and elongation in neurons, although not as potently as crmp2, and that this process is regulated by ser522/ser518/thr514/thr509 phosphorylation in both cases. We demonstrate that cdk5 primes crmp2 and crmp4 for subsequent phosphorylation by gsk3, whereas dyrk2, phosphorylates and primes only crmp4 in vitro

Identifier	Residue	Sequence	Organism
SIGNOR-145967	Thr509	PVFDLTTtPKGGTPA	Homo sapiens
pmid	sentence
16611631	Together, these results suggest that crmp4 is able to increase neurite formation and elongation in neurons, although not as potently as crmp2, and that this process is regulated by ser522/ser518/thr514/thr509 phosphorylation in both cases. We demonstrate that cdk5 primes crmp2 and crmp4 for subsequent phosphorylation by gsk3, whereas dyrk2, phosphorylates and primes only crmp4 in vitro

Identifier	Residue	Sequence	Organism
SIGNOR-145971	Thr514	TTTPKGGtPAGSARG	Homo sapiens
pmid	sentence
16611631	Together, these results suggest that crmp4 is able to increase neurite formation and elongation in neurons, although not as potently as crmp2, and that this process is regulated by ser522/ser518/thr514/thr509 phosphorylation in both cases. We demonstrate that cdk5 primes crmp2 and crmp4 for subsequent phosphorylation by gsk3, whereas dyrk2, phosphorylates and primes only crmp4 in vitro

Publications:

3

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-159314	Ser522	PAPSAKSsPSKHQPP	Homo sapiens	Neuron
pmid	sentence
18003833	These findings suggest that sema3a-induced spine development is regulated by phosphorylation of crmp1 by cdk5. Introduction of crmp1-wt, but not crmp1-t509a/s522a, a crmp1 mutant that cannot be phosphorylated by cdk5, rescued the defect in sema3a responsiveness.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-145912	Thr509	PVYEVPAtPKYATPA	Homo sapiens	Neuron
pmid	sentence
16611631	In summary, phosphorylation of thr509 of human crmp1 appears to be regulated by two mechanisms; direct phosphorylation by cdk5, or by priming of ser522 by cdk5 followed by sequential phosphorylation of ser518, thr514, and thr509 by gsk3.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-159318	Thr509	PVYEVPAtPKYATPA	Homo sapiens	Neuron
pmid	sentence
18003833	These findings suggest that sema3a-induced spine development is regulated by phosphorylation of crmp1 by cdk5. Introduction of crmp1-wt, but not crmp1-t509a/s522a, a crmp1 mutant that cannot be phosphorylated by cdk5, rescued the defect in sema3a responsiveness.

Publications:

3

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-264838	Ser522	PASSAKTsPAKQQAP	Homo sapiens	Neuron
pmid	sentence
25040932	Cdk5 and DYRK2 phosphorylate CRMP2 and CRMP4, respectively, priming these proteins at S522 before their subsequent phosphorylation by GSK-3b at T509, T516 and S518\|e CRMP2 phosphorylation by GSK-3b disrupts its interaction with tubulin (Yamashita & Goshima, 2012), leading to growth inhibition

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-78883	Ser551	PAARPPAsPSPQRQA	Homo sapiens
pmid	sentence
10880969	Synapsin i (syni), a major sv phosphoprotein involved in the regulation of sv trafficking and neurotransmitter release, is one of the presynaptic substrates of cdk5, which phosphorylates it in its c-terminal region at ser(549) (site 6) and ser(551) (site 7). Phosphorylation of syni by cdk5 is physiologically regulated and enhances its binding to f-actin.

Identifier	Residue	Sequence	Organism
SIGNOR-78887	Ser553	ARPPASPsPQRQAGP	Homo sapiens
pmid	sentence
10880969	Synapsin i (syni), a major sv phosphoprotein involved in the regulation of sv trafficking and neurotransmitter release, is one of the presynaptic substrates of cdk5, which phosphorylates it in its c-terminal region at ser(549) (site 6) and ser(551) (site 7). Phosphorylation of syni by cdk5 is physiologically regulated and enhances its binding to f-actin.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-276443	Ser557	LEEFDVFsPKQDLVP	Homo sapiens	HEK-293T Cell
pmid	sentence
25452387	The CDK5 kinase phosphorylates four serines in DLC1 located N-terminal to the Rho-GAP domain. When not phosphorylated, this N-terminal region functions as an autoinhibitory domain that places DLC1 in a closed, inactive conformation by efficiently binding to the Rho-GAP domain. CDK5 phosphorylation reduces this binding and orchestrates the coordinate activation DLC1, including its localization to focal adhesions, its Rho-GAP activity, and its ability to bind tensin and talin.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-276444	Ser642	DSFGSLPsPKELSSF	Homo sapiens	HEK-293T Cell
pmid	sentence
25452387	The CDK5 kinase phosphorylates four serines in DLC1 located N-terminal to the Rho-GAP domain. When not phosphorylated, this N-terminal region functions as an autoinhibitory domain that places DLC1 in a closed, inactive conformation by efficiently binding to the Rho-GAP domain. CDK5 phosphorylation reduces this binding and orchestrates the coordinate activation DLC1, including its localization to focal adhesions, its Rho-GAP activity, and its ability to bind tensin and talin.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-276445	Ser859	RRENSSDsPKELKRR	Homo sapiens	HEK-293T Cell
pmid	sentence
25452387	The CDK5 kinase phosphorylates four serines in DLC1 located N-terminal to the Rho-GAP domain. When not phosphorylated, this N-terminal region functions as an autoinhibitory domain that places DLC1 in a closed, inactive conformation by efficiently binding to the Rho-GAP domain. CDK5 phosphorylation reduces this binding and orchestrates the coordinate activation DLC1, including its localization to focal adhesions, its Rho-GAP activity, and its ability to bind tensin and talin.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-276446	Ser946	SVSPCPSsPKQIHLD	Homo sapiens	HEK-293T Cell
pmid	sentence
25452387	The CDK5 kinase phosphorylates four serines in DLC1 located N-terminal to the Rho-GAP domain. When not phosphorylated, this N-terminal region functions as an autoinhibitory domain that places DLC1 in a closed, inactive conformation by efficiently binding to the Rho-GAP domain. CDK5 phosphorylation reduces this binding and orchestrates the coordinate activation DLC1, including its localization to focal adhesions, its Rho-GAP activity, and its ability to bind tensin and talin.

Identifier	Residue	Organism
SIGNOR-279602		Homo sapiens
pmid	sentence
25452387	CDK5 kinase phosphorylates DLC1 but not DLC2 or DLC3 protein.\|Here, we report that CDK5 coordinately activates multiple DLC1 functions, elucidate the mechanism underlying this activation, and identify a role for DLC1 inactivation in the pro-oncogenic activity CDK5.

Publications:

5

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-278922	Ser56	SRSLYASsPGGVYAT	Homo sapiens
pmid	sentence
21465480	Cdk5 mediates vimentin Ser56 phosphorylation during GTP-induced secretion by neutrophils.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-278275	Ser616	PIPIMPAsPQKGHAV	Homo sapiens
pmid	sentence
25730670	CDK5 activates DRP1 in BTICs.\|To determine if CDK5 could directly phosphorylate DRP1, we performed an in vitro kinase assay with CDK5, its regulatory partner p25 and GST-DRP1 (wild type or S616A mutant) and found that CDK5 directly phosphorylates DRP1 on the S616 site (Fig. 7d).

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-134455	Ser650	DERSWVYsPLHYSAQ	Homo sapiens
pmid	sentence
15738269	The interaction of talin with phosphatidylinositol(4) phosphate 5 kinase type i gamma (pipki gamma) regulates pi(4,5)p2 synthesis at synapses and at focal adhesions. Here, we show that phosphorylation of serine 650 (s650) within the talin-binding sequence of human pipki gamma blocks this interaction. At synapses, s650 is phosphorylated by p35/cdk5 and mitogen-activated protein kinase at rest, and dephosphorylated by calcineurin upon stimulation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-249194	Ser67	LKSTLAMsPRQRKKM	Rattus norvegicus
pmid	sentence
11278334	In vitro and in vivo studies indicated that phospho-Ser-67 inhibitor-1 was dephosphorylated by protein phosphatases-2A and -2B. \| However, inhibitor-1 phosphorylated at Ser-67 was a less efficient substrate for cAMP-dependent protein kinase. These results demonstrate regulation of a Cdk5-dependent phosphorylation site in inhibitor-1 and suggest a role for this site in modulating the amplitude of signal transduction events that involve cAMP-dependent protein kinase activation.

Publications:

1

Organism:

Rattus Norvegicus

Identifier	Residue	Sequence	Organism
SIGNOR-264893	Ser68	PSDLSPEsPMLSSPP	in vitro
pmid	sentence
22577147	Altogether, these results indicate that CDK5 phosphorylates similarly serines 68 and 73, whereas ERK2 targets mostly serine 68 and GSK-3beta mostly serine 60.\|This observation may support the hypothesis of a specific localization of stathmin 3 depending on its phosphorylation by GSK-3beta

Identifier	Residue	Sequence	Organism
SIGNOR-264894	Ser73	PESPMLSsPPKKKDT	in vitro
pmid	sentence
22577147	Altogether, these results indicate that CDK5 phosphorylates similarly serines 68 and 73, whereas ERK2 targets mostly serine 68 and GSK-3beta mostly serine 60.\|This observation may support the hypothesis of a specific localization of stathmin 3 depending on its phosphorylation by GSK-3beta

Publications:

2

Organism:

In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-279020	Ser687	TEKSHPRsPNVLSVA	Homo sapiens
pmid	sentence
27027353	In conclusion, we obtained compelling evidence that CDK5 directly stabilizes the transcription factor hypoxia inducible factor-1\u03b1 by phosphorylation, and thus promotes the formation of blood vessels.\|Mass spectrometry and site directed mutagenesis revealed a stabilizing phosphorylation of HIF-1\u03b1 at Ser687 by CDK5.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-124325	Ser727	NTIDLPMsPRTLDSL	Homo sapiens	Neuron
pmid	sentence
15096606	We report here that the cdk5/p35 complex associates with stat3 and phosphorylates stat3 on the ser-727 residue in vitro and in vivo. Ser phosphorylation of stat3 and transcription of stat3 target genes, such as c-fos and junb, in a cdk5-dependent manner.

Publications:

1

Organism:

Homo Sapiens

Tissue:

Muscle, Myotube, Brain

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-86223	Ser732	SSEGFYPsPQHMVQT	Homo sapiens	Neuron
pmid	sentence
12941275	Here, we show that fak phosphorylation by cdk5 at s732 is important for microtubule organization, nuclear movement, and neuronal migration. In cultured neurons, s732-phosphorylated fak is enriched along a centrosome-associated microtubule fork that abuts the nucleus. Overexpression of the nonphosphorylatable mutant fak s732a results in disorganization of the microtubule fork and impairment of nuclear movement in vitro, and neuronal positioning defects in vivo.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-71950	Ser75	NSSDTVTsPQRAGPL	Homo sapiens	Neuron
pmid	sentence
10544291	These results present compelling evidence that cdk5/p35 kinase is responsible for the novel phosphorylation of c-src at ser75 in neuronal cells, raising the intriguing possibility that c-src acts as an effector of cdk5/p35 kinase during neuronal development.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-279153	Ser77	FPRRHYTsQQELKDE	Homo sapiens
pmid	sentence
21829588	Taken together, these sets of data suggest that Abeta triggers the phosphorylation of GKAP by cdk5 at the serine residues S77 and S111 that in turn are crucial for GKAP degradation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-250661	Ser774	SVPAGRRsPTSSPTP	in vitro
pmid	sentence
12855954	Here, we show that cyclin-dependent kinase 5 (Cdk5) phosphorylates dynamin I on Ser 774 and Ser 778 in vitro, which are identical to its endogenous phosphorylation sites in vivo. Cdk5 antagonists and expression of dominant-negative Cdk5 block phosphorylation of dynamin I, but not of amphiphysin or AP180, in nerve terminals and inhibit SVE.

Identifier	Residue	Sequence	Organism
SIGNOR-250662	Ser778	GRRSPTSsPTPQRRA	in vitro
pmid	sentence
12855954	Here, we show that cyclin-dependent kinase 5 (Cdk5) phosphorylates dynamin I on Ser 774 and Ser 778 in vitro, which are identical to its endogenous phosphorylation sites in vivo. Cdk5 antagonists and expression of dominant-negative Cdk5 block phosphorylation of dynamin I, but not of amphiphysin or AP180, in nerve terminals and inhibit SVE.

Publications:

2

Organism:

In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-276357	Ser782	YSLLRGGsDDSSKDP	in vitro
pmid	sentence
21922195	These results would suggest that the phosphorylation of PARP-1 via Cdk5's kinase activity is necessary for its persistence at damage sites.Based on these results and the recruitment data, we hypothesize that the phosphorylation of the PARP-1 protein by Cdk5 on one or more of the serines 782, 785, and 786 results in an attenuation of its ribosylating activity facilitating its persistence at the sites of DNA damage.

Identifier	Residue	Sequence	Organism
SIGNOR-276358	Ser785	LRGGSDDsSKDPIDV	in vitro
pmid	sentence
21922195	These results would suggest that the phosphorylation of PARP-1 via Cdk5's kinase activity is necessary for its persistence at damage sites.Based on these results and the recruitment data, we hypothesize that the phosphorylation of the PARP-1 protein by Cdk5 on one or more of the serines 782, 785, and 786 results in an attenuation of its ribosylating activity facilitating its persistence at the sites of DNA damage.

Identifier	Residue	Sequence	Organism
SIGNOR-276359	Ser786	RGGSDDSsKDPIDVN	in vitro
pmid	sentence
21922195	These results would suggest that the phosphorylation of PARP-1 via Cdk5's kinase activity is necessary for its persistence at damage sites.Based on these results and the recruitment data, we hypothesize that the phosphorylation of the PARP-1 protein by Cdk5 on one or more of the serines 782, 785, and 786 results in an attenuation of its ribosylating activity facilitating its persistence at the sites of DNA damage.

Publications:

3

Organism:

In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-280215	Ser789	QSVDKVTsPTKV	Homo sapiens
pmid	sentence
21791703	Together, these data demonstrate that phosphorylation of caldesmon on Ser527 by Cdk5 serves to down regulate its stability.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-183454	Ser794	LSNCTKKsPNKIASG	Homo sapiens	Neuron
pmid	sentence
19151707	Here we show that cdk5 (cyclin-dependent kinase 5), activated by dna damage, directly phosphorylates atm at ser 794 in post-mitotic neurons. Phosphorylation at ser 794 precedes, and is required for, atm autophosphorylation at ser 1981, and activates atm kinase activity

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-177963	Ser8	MGTVLSLsPSYRKAT	Homo sapiens
pmid	sentence
18326489	When overexpressed with cdk5, a large fraction of the double mutant p35(s8a/t138a) co-sedimented with microtubules (fig. 5b), further supporting the idea that the phosphorylation at these two residues by cdk5 is inhibitory to the microtubule association.

Identifier	Residue	Sequence	Organism
SIGNOR-177967	Thr138	PAVTSAGtPKRVIVQ	Homo sapiens
pmid	sentence
18326489	P35 phosphorylation by cdk5 interferes with the microtubule-binding and polymerizing activities of p35. Using a mutational approach, we found that only phosphorylation at thr-138, one of the two residues primarily phosphorylated in vivo, inhibits the polymerizing activity

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-134468	Ser811	IYISPLKsPYKISEG	Homo sapiens
pmid	sentence
15741232	Phosphorylation was observed 6 hours after p25 induction and was abolished in the presence of a cdk5 inhibitor, roscovitine, which does not inhibit the usual rb cyclin-d kinases cdk4 and cdk6. Furthermore, analyses of levels and subcellular localization of cdk-related cyclins did not reveal any change following cdk5 activation, arguing for a direct effect of cdk5 activity on rb protein. Rb phosphorylation was visualized using phosphorylation-dependent antibodies (p-rbser795 and p-rbser807/811).

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-175696	Ser83	QQQQQETsPRQQQQQ	Homo sapiens	Prostate Gland Cancer Cell
pmid	sentence
21799006	Cdk5 enables phosphorylation of ar at ser-81 site through direct biochemical interaction and, therefore, results in the stabilization of ar proteins

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-278921	Ser85	HQQPQSSsPVYGSSA	Homo sapiens
pmid	sentence
14970194	Thus, phosphorylation of paxillin is involved in NGF-induced neurite extension of PC-12 cells, probably through regulating focal adhesion organization.\|cdk5 and p38MAPK phosphorylates Ser 85 on paxillin in vitro.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-171138	Ser886	LSQSSDSsPTRNSEP	Homo sapiens	Macrophage
pmid	sentence
21220307	Ser(886) phosphorylation is required for the interaction of nsap1, which blocks eprs binding to target mrnas. The same phosphorylation event induces subsequent binding of ribosomal protein l13a and gapdh and restores mrna binding. Ifn-_ activates cdk5 to phosphorylate ser(886) in the linker domain of glutamyl-prolyl trna synthetase (eprs), the initial event in assembly of the gait complex. Cdk5/p35 also induces, albeit indirectly via a distinct kinase, phosphorylation of ser(999), the second essential event in gait pathway activation

Identifier	Residue	Sequence	Organism
SIGNOR-187383	Ser886	LSQSSDSsPTRNSEP	Homo sapiens
pmid	sentence
19647514	Ser(886) phosphorylation is required for the interaction of nsap1, which blocks eprs binding to target mrnas. The same phosphorylation event induces subsequent binding of ribosomal protein l13a and gapdh and restores mrna binding. Ifn-_ activates cdk5 to phosphorylate ser(886) in the linker domain of glutamyl-prolyl trna synthetase (eprs), the initial event in assembly of the gait complex. Cdk5/p35 also induces, albeit indirectly via a distinct kinase, phosphorylation of ser(999), the second essential event in gait pathway activation

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-278436	Thr1152	LDEEGYMtPMRDKPK	Homo sapiens
pmid	sentence
24142862	Cdk5 Promotes ErbB4 and PI3-Kinase Activity In Vivo.\|Cdk5 phosphorylates ErbB4 at T1152, situated in close proximity to the PI3-kinase-binding site (Y1056), and in turn promotes ErbB4 tyrosine phosphorylation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-250669	Thr1299	GETLPDStPLGFYLR	Mus musculus
pmid	sentence
12832492	We identify nestin as a novel in vivo target for cdk5 and p35 kinase, a critical signaling determinant in development. Two cdk5-specific phosphorylation sites on nestin, Thr-1495 and Thr-316, were established, the latter of which was used as a marker for cdk5-specific phosphorylation in vivo. \| Cdk5 activity is necessary for differentiation and the concomitant nestin reorganization in C2C12 myoblasts.

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250670	Thr315	AENSRLQtPGGGSKT	Mus musculus	C2C12 Cell
pmid	sentence
12832492	We identify nestin as a novel in vivo target for cdk5 and p35 kinase, a critical signaling determinant in development. Two cdk5-specific phosphorylation sites on nestin, Thr-1495 and Thr-316, were established, the latter of which was used as a marker for cdk5-specific phosphorylation in vivo. \| Cdk5 activity is necessary for differentiation and the concomitant nestin reorganization in C2C12 myoblasts.

Publications:

2

Organism:

Mus Musculus

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250668	Thr131	ISLLNVFtPQKTLEE	Homo sapiens	HEK-293 Cell
pmid	sentence
11823425	Here, we show that cdk5 directly phosphorylates c-Jun N-terminal kinase 3 (JNK3) on Thr131 and inhibits its kinase activity, leading to reduced c-Jun phosphorylation.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-170886	Thr135	TVQQHPStPKRHTVL	Homo sapiens	HEK-293 Cell
pmid	sentence
21209322	High nacl-induced activation of cdk5 increases phosphorylation of the osmoprotective transcription factor tonebp/orebp at threonine 135, which contributes to its rapid nuclear localization. n hek293 cells, mass spectrometry shows phosphorylation of tonebp/orebp-s120, -s134, -t135, and -s155.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-165772	Thr159	DGSEPTKtPGRTSST	Homo sapiens	Neuron
pmid	sentence
20513426	Thr159 phosphorylation negatively regulates the ptdins3 kinase activity of vps34 and autophagy cdk5/p25, a neuronal cdk shown to play a role in alzheimer's disease, can also phosphorylate thr159 of vps34.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-249328	Thr212	VIEPLPVtPTRDVAT	Chlorocebus aethiops	COS Cell
pmid	sentence
11604394	Our previous work revealed that the neuronal p35/Cdk5 kinase associates with Pak1 in a RacGTP-dependent manner, causing hyperphosphorylation and down-regulation of Pak1 kinase activity. We have now demonstrated direct phosphorylation of Pak1 on threonine 212 by the p35/Cdk5 kinase.

Publications:

1

Organism:

Chlorocebus Aethiops

Identifier	Residue	Sequence	Organism
SIGNOR-276337	Thr233	NKKNAGFtPQERQGF	Homo sapiens
pmid	sentence
21727086	Apurinic/apyrimidinic endonuclease-1 (APE1) is a multifunctional DNA repair/gene regulatory protein in mammalian cells, and was recently reported to be phosphorylated at Thr233 by CDK5.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250665	Thr235	YEKDDKLtPKIGFPW	Homo sapiens	SAOS-2 Cell
pmid	sentence
12769842	Increased ezrin expression and activation by CDK5 coincident with acquisition of the senescent phenotype.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-278249	Thr252	YTGSLWYtPIRREWY	Homo sapiens
pmid	sentence
26317805	BACE1 is phosphorylated by p25 and Cdk5 at Thr252.\|Our finding that p25/Cdk5 stimulates BACE1 activity supports that p25/Cdk5 may represent a promising target for the development of drugs to treat Alzheimer's disease.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-264406	Thr314	LPSEAGPtPCAPASF	Chlorocebus aethiops	COS Cell
pmid	sentence
30712943	Cyclin-dependent kinase 5 promotes proteasomal degradation of the 5-HT 1A receptor via phosphorylation\|5-HT1AR was phosphorylated by the Cdk5-p35 complex at Thr314 in the third cytoplasmic loop.

Publications:

1

Organism:

Chlorocebus Aethiops

Identifier	Residue	Sequence	Organism
SIGNOR-92269	Thr320	NPGGRPItPPRNSAK	Homo sapiens
pmid	sentence
12202491	Pp1 isoforms contain an arg-pro-ile/val-thr-pro-pro-arg sequence near the c terminus, a known site of phosphorylation by cdc/cdk kinases, and phosphorylation attenuates phosphatase activity. Increasing doses of cdk2 resulted in increased phosphorylation of the thr-320 site. Phosphorylation of this site in pp1 corresponded to decreased pp1 activity.

Identifier	Residue	Sequence	Organism
SIGNOR-151803	Thr320	NPGGRPItPPRNSAK	Homo sapiens
pmid	sentence
17202132	We observed that phosphorylation of protein phosphatase 1 (PP1) on Thr320 is reduced in brain extracts from Egr-1-/- mice, indicating that a kinase downstream of Egr-1 phosphorylates PP1. In HEK 293 cells co-transfected with PP1 and Cdk5, Cdk5 phosphorylates PP1. In vitro, Cdk5 purified from bovine brain phosphorylates bacterially expressed recombinant PP1

Publications:

2

Organism:

Homo Sapiens

Pathways:

Dopaminergic Synapse

Identifier	Residue	Sequence	Organism
SIGNOR-89145	Thr354	HLGPHRStPESRAAV	Homo sapiens
pmid	sentence
12056836	Cyclin-dependent kinase-5/p35 phosphorylates presenilin 1 to regulate carboxy-terminal fragment stabilityhere we demonstrate that cyclin dependent kinase-5/p35 (cdk5/p35) phosphorylates ps1 on threonine(354) within c-ps1 both in vitro and in vivo. Threonine(354) phosphorylation functions to selectively stabilize c-ps1.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-276672	Thr42	DELGKVLtPTQVKNR	Homo sapiens	HEK-293 Cell
pmid	sentence
25104559	Here, we demonstrate that RKIP is a substrate of cyclin-dependent kinase 5 (CDK5) in neurons and that the phosphorylation of RKIP at T42 causes the release of Raf-1. Moreover, T42 phosphorylation promotes the exposure and recognition of the target motif "KLYEQ" in the C-terminus of RKIP by chaperone Hsc70 and the subsequent degradation of RKIP via chaperone-mediated autophagy (CMA).

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-245187	Thr424	AAPEASGtPSSDAVS	Homo sapiens	MEL-JUSO Cell
pmid	sentence
26823173	We here show that phosphorylation of coronin 1 on Thr(418/424) by cyclin-dependent kinase (CDK) 5 activity was responsible for coronin 1-G_s association and the modulation of cAMP production. Together these results show an essential role for CDK5 activity in promoting the coronin 1-dependent cAMP/PKA pathway.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-203227	Thr451	AVSDPSStPTKIPTD	Homo sapiens
pmid	sentence
24235147	Cdk5 phosphorylates clock at the thr-451 and thr-461 residues in association with transcriptional activation of clock.

Identifier	Residue	Sequence	Organism
SIGNOR-203231	Thr461	KIPTDTStPPRQHLP	Homo sapiens
pmid	sentence
24235147	Cdk5 phosphorylates clock at the thr-451 and thr-461 residues in association with transcriptional activation of clock.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-262737	Thr506	SEGQVMLtPQKNTRT	Cricetulus griseus	CHO Cell
pmid	sentence
27512725	Overexpression of Cdk5 or its activator p35 promoted and inhibition of Cdk5 activity prevented the KIF13B-TRPV1 association, indicating that Cdk5 promotes TRPV1 anterograde transport by mediating the motor-cargo association. Cdk5 phosphorylates KIF13B at Thr-506, a residue located in the FHA domain. T506A mutation reduced the motor-cargo interaction and the cell-permeable TAT-T506 peptide, targeting to the Thr-506, decreased TRPV1 surface localization, demonstrating the essential role of Thr-506 phosphorylation in TRPV1 transport.

Publications:

1

Organism:

Cricetulus Griseus

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-157528	Thr572	IGSSHILtPTRFLDD	Homo sapiens	Neuron
pmid	sentence
17716669	It was shown that munc18 inhibition of neuronal syntaxin 1 can be overcome by cdk5 phosphorylation, indicating that structural change disrupts the syntaxin-munc18 interaction.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-259811	Thr668	ENLDLKLtPYKVLAT	Homo sapiens	HEK-293 Cell
pmid	sentence
20513426	Phosphorylation of Vps34 on Thr159 inhibits its interaction with Beclin 1. two additional amino acids in Vps34, Thr159 and Thr668, were found to be phosphorylated only after co-transfection with Cdk5/p25

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-277487	Thr724	KKKKKFRtPSFLKKS	Homo sapiens	MDA-MB-231 Cell
pmid	sentence
31548578	We found that Cdk5 directly phosphorylated the actin-binding protein adducin-1 (ADD1) at T724 in vitro and in intact cells.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-250672	Thr73	MKIDEPStPYHSMMG	in vitro
pmid	sentence
11320080	Neuronal Cdc2-like protein kinase (Cdk5/p25) is associated with protein phosphatase 1 and phosphorylates inhibitor-2. \| NCLK Phosphorylates Thr72 of I-2

Publications:

1

Organism:

In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-279364	Thr733	LPPVFSGtPKGSGAG	Homo sapiens
pmid	sentence
27735944	CDK5 directly phosphorylated ERK5 at Thr732 and modulated the ERK5\u2013AP-1 signaling axis.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250651	Thr743	VEVDAAVtPEERHLS	Rattus norvegicus	Neuron
pmid	sentence
10936190	In vitro, active cyclin-dependent kinase 5 (Cdk5) phosphorylated the cytoplasmic domain of APP at Thr(668). Treatment of mature neurons with an antisense oligonucleotide to Cdk5 suppressed Cdk5 expression and significantly diminished the level of phosphorylated APP. The expression of APP was unaffected in antisense-treated neurons. These results indicate that in neurons APP is phosphorylated by Cdk5, and that this may play a role in its localization.

Publications:

1

Organism:

Rattus Norvegicus

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-250671	Thr75	RPNPCAYtPPSLKAV	Rattus norvegicus	Brain
pmid	sentence
10604473	We find that DARPP-32 is converted into an inhibitor of PKA when phosphorylated at threonine 75 by cyclin-dependent kinase 5 (Cdk5). Cdk5 phosphorylates DARPP-32 in vitro and in intact brain cells. Phospho-Thr 75 DARPP-32 inhibits PKA in vitro by a competitive mechanism.

Publications:

1

Organism:

Rattus Norvegicus

Pathways:

Dopaminergic Synapse

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-277386	Thr77	LHSDKKLtLVFEFCD	Homo sapiens	DU-145 Cell
pmid	sentence
29511352	This generates a binding site for the C2 domain of PKCδ, which in turn phosphorylates CDK5 on T77. The resulting dissociation of the CDK5R1/CDK5 complex abolishes the activity of CDK5.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-251156	Tyr15	EKIGEGTyGTVFKAK	Homo sapiens
pmid	sentence
14757045	Constitutively active Fyn phosphorylated Tyr15 of Cdk5. Fyn Facilitates Kinase Activity of Cdk5 Via Tyr15 Phosphorylation

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-245288	Tyr15	EKIGEGTyGTVFKAK	Chlorocebus aethiops	COS-7 Cell
pmid	sentence
10896159	Phosphorylation of Cdk5 by c-Abl occurs on tyrosine 15 (Y15), which is stimulatory for p35/Cdk5 kinase activity.

Publications:

1

Organism:

Chlorocebus Aethiops

Identifier	Residue	Organism
SIGNOR-102652		Homo sapiens
pmid	sentence
12832520	Cprk displays catalytic activity in in vitro kinase assays and is itself phosphorylated by cdk5/p35. Cdk5/p35 inhibits cprk activity.

Identifier	Residue	Organism
SIGNOR-102717		Homo sapiens
pmid	sentence
12832520	Cprk displays catalytic activity in in vitro kinase assays and is itself phosphorylated by cdk5/p35. Cdk5/p35 inhibits cprk activity.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-250683		Homo sapiens
pmid	sentence
11331872	Induced p35 forms a complex with Cdk5 and activates its kinase activity

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-279022		Homo sapiens
pmid	sentence
15471880	In addition, we demonstrate that co-expression of cdk5 and its regulatory activator p35 with TH increases the stability of TH.\|We show that cdk5 phosphorylates TH at serine 31 and that this phosphorylation is associated with an increase in total TH activity.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-279021		Homo sapiens
pmid	sentence
28769056	Importantly, ephexin1, a Rho GEF, is phosphorylated by Cdk5 in vivo .

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-279155		Homo sapiens
pmid	sentence
26509276	Since Tyr-654 is the ERBB2 phosphorylation site on beta-catenin, this result is consistent with our hypothesis that CDK5 activates ERBB2 , which in turn phosphorylates beta-catenin on Tyr-654, leading to a shift of beta-catenin away from the adherens junction and into the nucleus where it can serve as a transcriptional co-activator.\|Taken together with the results of our kinase analysis, these observations suggest that CDK5 phosphorylation of both ERBB2 and ERBB3 and AR could drive a feedback loop, in which ERBB2 and ERBB3 promotes beta-catenin transcriptional activity that then contributes to higher expression of ERBB3.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-279683		Homo sapiens
pmid	sentence
28634551	Converse to the effect of PKA overexpression, overexpression of CDK5 and its activator, p35, decreased the association between spinophilin and NF-M as well as the expression of NF-M.\|Moreover, CDK5 phosphorylates NF-M [ xref ], and this was also apparent in our data, given a dramatic molecular weight shift in the NF-M band following CDK5 overexpression.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-279682		Homo sapiens
pmid	sentence
29742423	CDK5 Activates the Self-Renewal Regulator CREB1 in GSCs.\|Our data indicate that CDK5, which has previously been shown to activate CREB1 through cAMP and PKA in dopamine neurons present in the ventral tegmental area, can directly bind with and phosphorylate CREB1 in a PKA and cAMP independent manner, at least in GSCs.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Dopaminergic Synapse

Identifier	Residue	Organism
SIGNOR-279402		in vitro
pmid	sentence
20553580	In vitro kinase assays showed that Cdk5 directly phosphorylates PXR.\|Taken together, these data indicate that Cdk5 negatively regulates PXR activity, and that inhibition of Cdk5 is at least partially responsible for flavonoids induced activation of PXR.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Organism
SIGNOR-279401		Homo sapiens
pmid	sentence
33960694	An in vitro kinase reaction demonstrated that T2132, S2136, and S2141 were CDK5\u2010phosphorylated sites in the Notch1 peptide (Figure\u00a02B, C, and D).\|In conclusion, CDK5 positively regulates Notch1 function via phosphorylation, which in turn promotes cell proliferation and migration.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-279365		Homo sapiens
pmid	sentence
24662752	GST-Sox6 was phosphorylated in vitro by Cdk5 and p35 (XREF_FIG).\|Inhibition of Cdk5 activity by DN Cdk5 and roscovitine increases the Sox6 expression in primary cortical neurons.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-279154		Homo sapiens
pmid	sentence
25452387	CDK5 activates the tumor suppressor DLC1 by phosphorylating and diminishing the binding of an autoinhibitory region of DLC1 to its Rho-GAP domain and allows it to localize to focal adhesions.\|Here, we report that CDK5 coordinately activates multiple DLC1 functions, elucidate the mechanism underlying this activation, and identify a role for DLC1 inactivation in the pro oncogenic activity CDK5.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-264649		Homo sapiens
pmid	sentence
12202491	Pp1 isoforms contain an arg-pro-ile/val-thr-pro-pro-arg sequence near the c terminus, a known site of phosphorylation by cdc/cdk kinases, and phosphorylation attenuates phosphatase activity. Increasing doses of cdk2 resulted in increased phosphorylation of the thr-320 site. Phosphorylation of this site in pp1 corresponded to decreased pp1 activity.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-279603		Homo sapiens
pmid	sentence
18628310	We then demonstrated that Cdk5 phosphorylates Kalirin 7 on Thr 1590 , increasing its GEF activity slightly and changing its solubility properties.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-279157		Homo sapiens
pmid	sentence
26912996	CDK5 increases recombinant SYNGAP1 activity on Ras-GAP by 98% and its Rap-GAP activity by 20%.\|Interestingly, phosphorylation of SYNGAP1 by CDK5 and CaMKII increases overall SYNGAP1 activity, but also alters the ratio of its GAP activity towards Ras- and Rap-GTPases.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-279679		Homo sapiens
pmid	sentence
22836916	Using both the Cdk inhibitor roscovitine and an RNA interference strategy, it was also demonstrated that Cdh1 was phosphorylated by Cdk5, an enzyme that can be persistently activated when bound to p25 [ xref ], the proteolytic product of p35 that has previously been shown to accumulate in the neurons of patients with Alzheimer\u2019s disease [ xref ].

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-279323		Homo sapiens
pmid	sentence
20573893	Cdk5 mediated delta-catenin phosphorylation regulates delta-catenin subcellular localization into two distinct pools : a cytoplasmic or intraneurite state as well as a pool that is localized to the membrane.\|Cdk5 phosphorylates delta-catenin on serines 300 and 357.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-206574		Homo sapiens
pmid	sentence
Other

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-278920		Homo sapiens
pmid	sentence
19587281	Cdk5 phosphorylated PrP induces the aggregation of non phosphorylated PrP.\|Together, these results indicate that S43 is a major Cdk5 phosphorylation site in PrP.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-278437		Homo sapiens
pmid	sentence
26894912	TNF-alpha overexpression increased Cdk5-mediated phosphorylation of TRPV1 at T407.\|These results suggest that the activation of Cdk5 by p35 enhances the response of TRPV1 to capsaicin, probably by phosphorylation of the channel [34].

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-192104		Homo sapiens
pmid	sentence
Other

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-189993		Homo sapiens
pmid	sentence
Other

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-279149		Homo sapiens
pmid	sentence
12084709	Taken together, our findings demonstrate that Pctaire1 interacts with p35, both in vitro and in vivo, and that phosphorylation of Pctaire1 by Cdk5 enhances its kinase activity.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-279156		Homo sapiens
pmid	sentence
26327394	Cdk5 phosphorylates Foxc2 and activates Foxc2 dependent transcription.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-206133		Homo sapiens
pmid	sentence
Other

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-123387		Homo sapiens
pmid	sentence
15013773	In brain, p35 or p25 exists with and activates cdk5

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-280221		Homo sapiens
pmid	sentence
25831123	Finally, threonine 222 of XOR is the critical target site for CDK5 dependent activation of XOR.\|Once we determined CDK5 was necessary for hypoxia induced hyperactivation of XOR, we tested whether CDK5 was sufficient to phosphorylate XOR and induce increased enzymatic activity in a cell free system.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-280220		Homo sapiens
pmid	sentence
15331630	Roscovitine inhibits the ability of Trio to activate Rac, and peptides corresponding to the Cdk5 consensus sites in Trio are phosphorylated by Cdk5.\|Together, these data suggest that control of the cortical actin cytoskeleton, long known to modulate hormone exocytosis and subsequent endocytosis, involves Cdk5 mediated activation of Trio.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-280219		Homo sapiens
pmid	sentence
28502042	Cdk5 also phosphorylates PSD-95-interacting protein Spine Associated RapGAP (SPAR), resulting in its degradation ([98], Table 2).

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-192467		Homo sapiens
pmid	sentence
Other

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-280218		Homo sapiens
pmid	sentence
31786229	In vitro, the results show that murine wild-type AMPK-alpha2 was phosphorylated by Cdk5 at a (S/T) PX (K/H/R) phosphorylation consensus sequence, which was associated with decreased AMPK-alpha2 activity.\|Inactivated AMPK-alpha2 promotes the progression of diabetic brain damage by Cdk5 phosphorylation at Thr485 site.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-280217		Homo sapiens
pmid	sentence
21763614	Similar to the mechanism of PAR-1 regulation of Mib in neurogenesis, CDK5 phosphorylation is proposed to enhance Mib1 ligase activity leading to destabilization.\|The cyclin dependent kinase 5 (CDK5) enriched in neurons phosphorylates Mib1 and suppresses the inhibitory effects of Mib1 on neurite morphology.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-191328		Homo sapiens
pmid	sentence
Other

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-280216		Homo sapiens
pmid	sentence
18054859	Cdk5 promotes synaptogenesis by regulating the subcellular distribution of the MAGUK family member CASK.\|We found that Cdk5 phosphorylates and regulates CASK distribution to membranes.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-268153		Homo sapiens	Neuron
pmid	sentence
10604467	Cyclin-dependent kinase 5 (Cdk5) is required for proper development of the mammalian central nervous system. To be activated, Cdk5 has to associate with its regulatory subunit, p35. We have found that p25, a truncated form of p35, accumulates in neurons in the brains of patients with Alzheimer's disease. This accumulation correlates with an increase in Cdk5 kinase activity. Unlike p35, p25 is not readily degraded, and binding of p25 to Cdk5 constitutively activates Cdk5, changes its cellular location and alters its substrate specificity.

Publications:

1

Organism:

Homo Sapiens

Name	CDK5 View Modifications
Full Name	Cyclin-dependent-like kinase 5
Synonyms	Cell division protein kinase 5, Serine/threonine-protein kinase PSSALRE, Tau protein kinase II catalytic subunit, TPKII catalytic subunit \| CDKN5
Primary ID	Q00535
Links	- -
Type	protein
Relations	183
Pathways	Dopaminergic Synapse
Inhibitors	seliciclib; alvocidib; 4-(2,6-dichlorobenzamido)-N-(piperidin-4-yl)-pyrazole-3-carboxamide; N-[6,6-dimethyl-5-[(1-methyl-4-piperidinyl)-oxomethyl]-1,4-dihydropyrrolo[3,4-c]pyrazol-3-yl]-3-methylbutanamide; alvocidib hydrochloride; Dinaciclib
Function	Proline-directed serine/threonine-protein kinase essential for neuronal cell cycle arrest and differentiation and may be involved in apoptotic cell death in neuronal diseases by triggering abortive cell cycle re-entry. Interacts with D1 and D3-type G1 cyclins. Phosphorylates SRC, NOS3, VIM/vimentin, p35/CDK5R1, MEF2A, SIPA1L1, SH3GLB1, PXN, PAK1, MCAM/MUC18, SEPT5, SYN1, DNM1, AMPH, SYNJ1, CDK16, RAC1, RHOA, CDC42, TONEBP/NFAT5, MAPT/TAU, MAP1B, histone H1, p53/TP53, HDAC1, APEX1, PTK2/FAK1, huntingtin/HTT, ATM, MAP2, NEFH and NEFM. Regulates several neuronal development and physiological processes including neuronal survival, migration and differentiation, axonal and neurite growth, synaptogenesis, oligodendrocyte differentiation, synaptic plasticity and neurotransmission, by phosphorylating key proteins. Activated by interaction with CDK5R1 (p35) and CDK5R2 (p39), especially in post-mitotic neurons, and promotes CDK5R1 (p35) expression in an autostimulation loop. Phosphorylates many downstream substrates such as Rho and Ras family small GTPases (e.g. PAK1, RAC1, RHOA, CDC42) or microtubule-binding proteins (e.g. MAPT/TAU, MAP2, MAP1B), and modulates actin dynamics to regulate neurite growth and/or spine morphogenesis. Phosphorylates also exocytosis associated proteins such as MCAM/MUC18, SEPT5, SYN1, and CDK16/PCTAIRE1 as well as endocytosis associated proteins such as DNM1, AMPH and SYNJ1 at synaptic terminals. In the mature central nervous system (CNS), regulates neurotransmitter movements by phosphorylating substrates associated with neurotransmitter release and synapse plasticity; synaptic vesicle exocytosis, vesicles fusion with the presynaptic membrane, and endocytosis. Promotes cell survival by activating anti-apoptotic proteins BCL2 and STAT3, and negatively regulating of JNK3/MAPK10 activity. Phosphorylation of p53/TP53 in response to genotoxic and oxidative stresses enhances its stabilization by preventing ubiquitin ligase-mediated proteasomal degradation, and induces transactivation of p53/TP53 target genes, thus regulating apoptosis. Phosphorylation of p35/CDK5R1 enhances its stabilization by preventing calpain-mediated proteolysis producing p25/CDK5R1 and avoiding ubiquitin ligase-mediated proteasomal degradation. During aberrant cell-cycle activity and DNA damage, p25/CDK5 activity elicits cell-cycle activity and double-strand DNA breaks that precedes neuronal death by deregulating HDAC1. DNA damage triggered phosphorylation of huntingtin/HTT in nuclei of neurons protects neurons against polyglutamine expansion as well as DNA damage mediated toxicity. Phosphorylation of PXN reduces its interaction with PTK2/FAK1 in matrix-cell focal adhesions (MCFA) during oligodendrocytes (OLs) differentiation. Negative regulator of Wnt/beta-catenin signaling pathway. Activator of the GAIT (IFN-gamma-activated inhibitor of translation) pathway, which suppresses expression of a post-transcriptional regulon of proinflammatory genes in myeloid cells; phosphorylates the linker domain of glutamyl-prolyl tRNA synthetase (EPRS) in a IFN-gamma-dependent manner, the initial event in assembly of the GAIT complex. Phosphorylation of SH3GLB1 is required for autophagy induction in starved neurons. Phosphorylation of TONEBP/NFAT5 in response to osmotic stress mediates its rapid nuclear localization. MEF2 is inactivated by phosphorylation in nucleus in response to neurotoxin, thus leading to neuronal apoptosis. APEX1 AP-endodeoxyribonuclease is repressed by phosphorylation, resulting in accumulation of DNA damage and contributing to neuronal death. NOS3 phosphorylation down regulates NOS3-derived nitrite (NO) levels. SRC phosphorylation mediates its ubiquitin-dependent degradation and thus leads to cytoskeletal reorganization. May regulate endothelial cell migration and angiogenesis via the modulation of lamellipodia formation. Involved in dendritic spine morphogenesis by mediating the EFNA1-EPHA4 signaling. The complex p35/CDK5 participates in the regulation of the circadian clock by modulating the function of CLOCK protein

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