| + |
HIF1AN | down-regulates 
hydroxylation
|
NOTCH1 |
0.552 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-161057 |
Asn1955 |
LEASADAnIQDNMGR |
Homo sapiens |
|
| pmid |
sentence |
| 18299578 |
We show that fih-1 hydroxylates notch icd at two residues (n(1945) and n(2012)) that are critical for the function of notch icd as a transactivator within cells and during neurogenesis and myogenesis in vivo. Fih-1 negatively regulates notch activity and accelerates myogenic differentiation. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-161061 |
Asn2022 |
INSHADVnAVDDLGK |
Homo sapiens |
|
| pmid |
sentence |
| 18299578 |
We show that fih-1 hydroxylates notch icd at two residues (n(1945) and n(2012)) that are critical for the function of notch icd as a transactivator within cells and during neurogenesis and myogenesis in vivo. Fih-1 negatively regulates notch activity and accelerates myogenic differentiation. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
EIF3F | up-regulates 
deubiquitination
|
NOTCH1 |
0.423 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-170158 |
Lys1759 |
CGVLLSRkRRRQHGQ |
Homo sapiens |
|
| pmid |
sentence |
| 21124883 |
The activated form of notch needs to be deubiquitinated before being processed by the gamma-secretase activity and entering the nucleus, where it fulfills its transcriptional function. The enzyme accounting for this deubiquitinase activity is eif3f, known so far as a translation initiation factor. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KAT5 | down-regulates
acetylation
|
NOTCH1 |
0.416 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-156911 |
Lys2029 |
NAVDDLGkSALHWAA |
Homo sapiens |
|
| pmid |
sentence |
| 17636029 |
This result implies that the residues k2019, k2039, k2044, and k2068 of notch1-ic are the major targets of the acetyltransferase activity of tip60. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-156915 |
Lys2049 |
DAAVVLLkNGANKDM |
Homo sapiens |
|
| pmid |
sentence |
| 17636029 |
This result implies that the residues k2019, k2039, k2044, and k2068 of notch1-ic are the major targets of the acetyltransferase activity of tip60. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-156919 |
Lys2054 |
LLKNGANkDMQNNRE |
Homo sapiens |
|
| pmid |
sentence |
| 17636029 |
This result implies that the residues k2019, k2039, k2044, and k2068 of notch1-ic are the major targets of the acetyltransferase activity of tip60. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-156923 |
Lys2078 |
EGSYETAkVLLDHFA |
Homo sapiens |
|
| pmid |
sentence |
| 17636029 |
This result implies that the residues k2019, k2039, k2044, and k2068 of notch1-ic are the major targets of the acetyltransferase activity of tip60. |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
PLK1 | down-regulates quantity by destabilization
phosphorylation
|
NOTCH1 |
0.404 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277491 |
Ser1791 |
REPLGEDsVGLKPLK |
Homo sapiens |
HaCaT Cell |
| pmid |
sentence |
| 31597699 |
As shown in Fig. S4D, the C-terminal NOTCH1 fragment was readily phosphorylated by PLK1. Additionally, when the two putative phosphorylation sites, Ser-1791 and Ser-2349, were replaced by Ala, WT NOTCH1-IC but not the mutant was efficiently phosphorylated (Fig. S4E). We found that mutation of Ser-1791/2349 promotes NOTCH1-IC stabilization (Fig. S4F). |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277490 |
Ser2439 |
SFLSGEPsQADVQPL |
Homo sapiens |
HaCaT Cell |
| pmid |
sentence |
| 31597699 |
As shown in Fig. S4D, the C-terminal NOTCH1 fragment was readily phosphorylated by PLK1. Additionally, when the two putative phosphorylation sites, Ser-1791 and Ser-2349, were replaced by Ala, WT NOTCH1-IC but not the mutant was efficiently phosphorylated (Fig. S4E). We found that mutation of Ser-1791/2349 promotes NOTCH1-IC stabilization (Fig. S4F). |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
CDK3 | down-regulates quantity by destabilization
phosphorylation
|
NOTCH1 |
0.244 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273169 |
Ser2513 |
EHPFLTPsPESPDQW |
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273168 |
Ser2516 |
FLTPSPEsPDQWSSS |
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273167 |
Thr2511 |
VPEHPFLtPSPESPD |
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Publications: |
3 |
Organism: |
In Vitro |
| + |
CDK8 | down-regulates quantity by destabilization
phosphorylation
|
NOTCH1 |
0.55 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273176 |
Ser2513 |
EHPFLTPsPESPDQW |
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273177 |
Ser2516 |
FLTPSPEsPDQWSSS |
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273178 |
Thr2511 |
VPEHPFLtPSPESPD |
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Publications: |
3 |
Organism: |
In Vitro |
| + |
CDK19 | down-regulates quantity by destabilization
phosphorylation
|
NOTCH1 |
0.303 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273136 |
Ser2513 |
EHPFLTPsPESPDQW |
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273135 |
Ser2516 |
FLTPSPEsPDQWSSS |
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273137 |
Thr2511 |
VPEHPFLtPSPESPD |
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Publications: |
3 |
Organism: |
In Vitro |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
HEY1 |
0.774 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-235397 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 11486044 |
These data establish that HERP2 is a novel primary target gene of Notch that, together with HES, may effect diverse biological activities of Notch |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | NOTCH Signaling, NOTCH Signaling and Myogenesis |
| + |
CyclinC/CDK19 | down-regulates quantity by destabilization
phosphorylation
|
NOTCH1 |
0.39 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273163 |
|
|
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273161 |
|
|
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273162 |
|
|
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Publications: |
3 |
Organism: |
In Vitro |
| + |
KAT2B | up-regulates
acetylation
|
NOTCH1 |
0.598 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-199024 |
|
|
Homo sapiens |
T-lymphocyte, Leukemia Cell |
| pmid |
sentence |
| 23029358 |
In earlier studies, we demonstrated that maml1 enhanced p300 acetyltransferase activity, which increased the acetylation of notch by p300.Acetylation controls notch stability and function in t-cell leukemia. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-177749 |
|
|
Homo sapiens |
T-lymphocyte, Leukemia Cell |
| pmid |
sentence |
| 22120716 |
In earlier studies, we demonstrated that maml1 enhanced p300 acetyltransferase activity, which increased the acetylation of notch by p300.Acetylation controls notch stability and function in t-cell leukemia. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
NOTCH1 | up-regulates quantity by expression 
transcriptional regulation
|
IL2RA |
0.297 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-80336 |
|
|
Homo sapiens |
Thymoma Cell |
| pmid |
sentence |
| 10933396 |
Activation of notch1 signaling in dp thymocytes and thymoma cell lines results in the upregulation of cd25 and cd44 expression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DLL1 | up-regulates activity
binding
|
NOTCH1 |
0.624 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-209732 |
|
|
Homo sapiens |
B-lymphocyte |
| pmid |
sentence |
| 16140393 |
Notch signaling is a highly conserved pathway involved in cell fate choice during development with Delta and Jagged constituting the two evolutionary conserved families of Notch ligands. These ligands are transmembrane proteins with conserved biochemical structure that share their receptors and signal through a common mechanism. Upon ligand binding Notch receptors are proteoliticaly cleaved, the intracellular domain of Notch (NICD) is released and translocated to the nucleus, where it activates target genes. In mammals, four receptors and five ligands have been described. Delta-1, Delta-3 and Delta-4 are homologues to Drosophila Delta and Jagged-1 and Jagged-2 to Drosophila Serrate. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | NOTCH Signaling, NOTCH Signaling and Myogenesis, Rett syndrome |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
NOTCH1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-149777 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 16990763 |
Other notch target genes identi?ed In the thymoma cell line were dtx1 (gene for deltex1), i?-202, i?-204, i?-D3, adam19 (meltrinb).24 a number of other genes have been reported as being notch targets, including notch1 itself,28 nrarp in xenopus embryos,29 bcl2 in thymoma cells,30 ccnd1 (gene for cyclin d1) in a kidney cell line,31 dkn1a (gene for cyclindependent kinase inhibitor 1a (p21, cip1)) in keratinocytes32 and tcf3 (gene for e2a). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, FLT3-ITD signaling, NOTCH Signaling, NOTCH Signaling and Myogenesis, Retinoic acid Signaling, Rett syndrome |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
IL7R |
0.324 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-197452 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 22577461 |
E2a positively regulates notch1 expression, which induces the expression of hebalt, bcl11b, and il7r. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
BCL11B |
0.396 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-197449 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 22577461 |
E2a positively regulates notch1 expression, which induces the expression of hebalt, bcl11b, and il7r. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KPNA6 | up-regulates
relocalization
|
NOTCH1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-165343 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20454918 |
Nicd binds via one of its four potential nuclear localization signals to importins alfa3, alfa4, and alfa7. importins alpha3, alpha4 (and to a lesser extent, alpha7) mediate nuclear import of nicd and thus are directly involved in notch signaling. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
ADAM19 |
0.312 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-80330 |
|
|
Homo sapiens |
T-lymphocyte, Thymoma Cell |
| pmid |
sentence |
| 10933396 |
Deltex, meltrin beta, ifi-202, and ifi-204 were also upregulated by notchic in the 2b4.11 t cell hybridoma, whereas ifi-d3 was expressed constitutively at relatively high levels and slightly upregulated by notchic, and pre-talfa was not expressed. Deltex, meltrin beta, pre-talfa, ifi-202, and ifi-204 were upregulated by notchic expression in the akr1 dp thymoma cell line, whereas ifi-d3 was not expressed |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KPNA4 | up-regulates
relocalization
|
NOTCH1 |
0.288 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-165314 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20454918 |
Nicd binds via one of its four potential nuclear localization signals to importins alfa3, alfa4, and alfa7. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
CD44 |
0.42 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-80333 |
|
|
Homo sapiens |
Thymoma Cell |
| pmid |
sentence |
| 10933396 |
Activation of notch1 signaling in dp thymocytes and thymoma cell lines results in the upregulation of cd25 and cd44 expression |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DTX1 | up-regulates activity
ubiquitination
|
NOTCH1 |
0.78 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236870 |
|
|
Mus musculus |
C2C12 Cell |
| pmid |
sentence |
| 11226752 |
Murine homologs of deltex define a novel gene family involved in vertebrate Notch signaling and neurogenesis |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-219269 |
|
|
Drosophila melanogaster |
|
| pmid |
sentence |
| 22162134 |
The expression of dx, which physically interacts with notch, favors a mono-ubiquitinated state of the receptor, which leads to a ligand-independent intracellular activation of notch |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-85942 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11153911 |
The human Deltex (DTX1) gene encodes a cytoplasmic protein that functions as a positive regulator of the Notch signaling pathway. |
|
| Publications: |
3 |
Organism: |
Mus Musculus, Drosophila Melanogaster, Homo Sapiens |
| Pathways: | NOTCH Signaling, NOTCH Signaling and Myogenesis |
| + |
DLK2 | down-regulates
binding
|
NOTCH1 |
0.291 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-172864 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21419176 |
In this work, we demonstrate, for the first time, that dlk2 interacts with itself, with dlk1, and with the same notch1 receptor region as dlk1 does. We demonstrate also that the interaction of dlk2 with notch1 similarly results in an notch signaling in preadipocytes and mouse embryo fibloblasts. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JAG2 | up-regulates
binding
|
NOTCH1 |
0.621 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236922 |
|
|
Mus musculus |
C2C12 Cell, Myoblast |
| pmid |
sentence |
| 9315665 |
Immunohistochemistry revealed coexpression of jagged2 and notch1 within thymus and other fetal murine tissues, consistent with interaction of the two proteins in vivo. Coculture of fibroblasts expressing human jagged2 with murine c2c12 myoblasts inhibited myogenic differentiation, accompanied by increased notch1 and the appearance of a novel 115-kda notch1 fragment. Exposure of c2c12 cells to jagged2 led to increased amounts of notch mrna as well as mrnas for a second notch receptor, notch3, and a second notch ligand, jagged1. Constitutively active forms of notchl in c2c12 cells also induced increased levels of the same set of mrnas, suggesting positive feedback control of these genes initiated by binding of jagged2 to notch1. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | NOTCH Signaling |
| + |
MAPK8IP1 | down-regulates
binding
|
NOTCH1 |
0.267 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-165710 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20508646 |
Here, we show that jip1 suppresses notch1 activity. Jip1 was found to physically associate with either intracellular domain of notch1 or rbp-jk and interfere with the interaction between them. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CyclinC/CDK3 | down-regulates quantity by destabilization
phosphorylation
|
NOTCH1 |
0.36 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273164 |
|
|
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273165 |
|
|
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273166 |
|
|
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Publications: |
3 |
Organism: |
In Vitro |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
LFNG |
0.756 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236845 |
|
|
Mus musculus |
C2C12 Cell |
| pmid |
sentence |
| 15207708 |
Notch signal transduction pathway genes, lfng, hey1, and hes1, are differen-tially regulated by bmp-2 and tgf-beta. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-195621 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22298955 |
Notch signal transduction pathway genes, lfng, hey1, and hes1, are differen-tially regulated by bmp-2 and tgf-beta. |
|
| Publications: |
2 |
Organism: |
Mus Musculus, Homo Sapiens |
| + |
JAG1 | up-regulates activity
binding
|
NOTCH1 |
0.639 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-219253 |
|
|
Drosophila melanogaster |
|
| pmid |
sentence |
| 18660822 |
We identify functional fragments of human notch-1 (n-1) and jagged-1 (j-1) which interact in a calcium-dependent manner. |
|
| Publications: |
1 |
Organism: |
Drosophila Melanogaster |
| Pathways: | NOTCH Signaling |
| + |
HEY2 | down-regulates
binding
|
NOTCH1 |
0.768 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-146690 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16682003 |
Here we show that hrt2 and hes1 interact with rbp-jkappa to negatively regulate notch-dependent activation of hrt and hes expression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
FABP7 |
0.545 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-145365 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16554461 |
Here we demonstrate that neuronal induction of radial glia formation is the result of sequential signaling through notch1 and erbb receptors. First, notch1 activation by neuronal contact induces the glial expression of the brain lipid binding protein (blbp) and erbb2 genes. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
YY1 | down-regulates activity
binding
|
NOTCH1 |
0.62 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251654 |
|
|
Homo sapiens |
K-562 Cell |
| pmid |
sentence |
| 12913000 |
Taken together, these results indicate that transcription factor YY1 may modulate Notch signaling via association with the high molecular weight Notch complex [..] both YY1 and N1IC were present in a large complex of the nucleus to suppress the luciferase reporter activity transactivated by Notch signaling. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | NOTCH Signaling |
| + |
MAML2 | up-regulates quantity by expression
transcriptional regulation
|
NOTCH1 |
0.837 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-94065 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12370315 |
We recently cloned a mammalian homologue of the mastermind gene of drosophila melanogaster, maml1 (mastermind-like-1 molecule) and determined that it functions as a transcriptional coactivator for notch receptors. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CCNC | down-regulates
phosphorylation
|
NOTCH1 |
0.477 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-130592 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15546612 |
Purified recombinant cycc:cdk8 phosphorylates the notch icd within the tad and pest domains, and expression of cycc:cdk8 strongly enhances notch icd hyperphosphorylation and pest-dependent degradation by the fbw7/sel10 ubiquitin ligase in vivo. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
NOTCH1 |
0.479 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253606 |
|
|
Homo sapiens |
Rheumatoid Arthritis Disease Specific Synovial Fibroblast |
| pmid |
sentence |
| 14586405 |
We found that TNF induced the expression of Notch-1, Notch-4, and Jagged-2 in RSF. The expression of these proteins was detected in the RA synovial tissues. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MFNG | up-regulates
binding
|
NOTCH1 |
0.718 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-80555 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10935626 |
Manic fringe elongates the o-linked fucose saccharides on full-length notch1 and notch1 egf repeats 1923. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DYRK1A | down-regulates
phosphorylation
|
NOTCH1 |
0.399 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-185494 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19383720 |
Dyrk1a physically interacts with the nicd inducing its phosphorylation in the ankyrin domain, thereby attenuating notch . |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Brain |
| + |
TCF3 | up-regulates quantity by expression
transcriptional regulation
|
NOTCH1 |
0.43 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-197523 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 22577461 |
E2a positively regulates notch1 expression, which induces the expression of hebalt, bcl11b, and il7r. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DLK2 | down-regulates activity
binding
|
NOTCH1 |
0.291 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-219377 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 21419176 |
Moreover, the interaction of DLK1 with NOTCH1 caused an inhibition of basal NOTCH signaling in preadipocytes and mesenchymal multipotent cells. In this work, we demonstrate, for the first time, that DLK2 interacts with itself, with DLK1, and with the same NOTCH1 receptor region as DLK1 does. We demonstrate also that the interaction of DLK2 with NOTCH1 similarly results in an inhibition of NOTCH signaling in preadipocytes and Mouse Embryo fibloblasts. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Tissue: |
MEF Cell |
| + |
SIAH1 | up-regulates
relocalization
|
NOTCH1 |
0.261 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-168460 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20940030 |
The overexpression of siah1 causes the re-localization of notch from the cell surface to the cytoplasm and to the nucleus, which is indicative of notch activation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SIRT1 | down-regulates
deacetylation
|
NOTCH1 |
0.428 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-195333 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22223095 |
The acetylation marks on notch1-icd are removed by the deacetylase sirt1, suggesting that both deacetylation of notch1-icd and of histones inhibit notch signaling. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
CKM complex | down-regulates quantity by destabilization
phosphorylation
|
NOTCH1 |
0.383 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273150 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15546612 |
Purified recombinant cycc:cdk8 phosphorylates the notch icd within the tad and pest domains, and expression of cycc:cdk8 strongly enhances notch icd hyperphosphorylation and pest-dependent degradation by the fbw7/sel10 ubiquitin ligase in vivo. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273160 |
|
|
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273159 |
|
|
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273158 |
|
|
in vitro |
|
| pmid |
sentence |
| 25344755 |
Mapping of cyclin C-dependent phosphosites on ICN1, using mass spectrometry revealed that several of them are located within the PEST-domain of Notch1, which controls ICN1 degradation38,39 (Fig. 5g and Supplementary Table 1). Three of them (T2512, S2514 and S2517) are localized within the consensus motif, “Cdc4 phosphodegron”, which is shared by most substrates of Fbw7 (Cdc4) ubiquitin ligase38. Two of these residues (S2514 and S2517) were previously shown by Fryer et al.20 to be phosphorylated by cyclin C-CDK8 in vitro, and all three were shown to play a role in controlling ICN1 stability via Fbw740. We verified that cyclin C-CDK8, C-CDK19 and C-CDK3 phosphorylate ICN1 on these three residues |
|
| Publications: |
4 |
Organism: |
Homo Sapiens, In Vitro |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
MYC |
0.67 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-147944 |
|
|
Homo sapiens |
T-lymphocyte, Leukemia Cell, Lymphoma Cell |
| pmid |
sentence |
| 16847353 |
We identified c-myc as a direct target of notch1 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, FLT3-ITD signaling, NOTCH Signaling |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
PPARG |
0.342 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-90455 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12107827 |
Addition of jag-1 peptide induced ikkalpha mediated nf-kappab activation, as well as increased ppargamma expression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Skin |
| Pathways: | Rett syndrome |
| + |
ITCH | down-regulates
ubiquitination
|
NOTCH1 |
0.641 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-80702 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10940313 |
Itch binds to the n-terminal portion of the notch intracellular domain via its ww domains and promotes ubiquitination of notch through its hect ubiquitin ligase domain. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Skin |
| + |
SNW1 | up-regulates activity
binding
|
NOTCH1 |
0.599 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-237617 |
|
|
in vitro |
|
| pmid |
sentence |
| 10713164 |
SKIP, a CBF1-associated protein, interacts with the ankyrin repeat domain of NotchIC To facilitate NotchIC function. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
DLK1 | down-regulates activity
binding
|
NOTCH1 |
0.514 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-172830 |
|
|
Mus musculus |
MEF Cell |
| pmid |
sentence |
| 21419176 |
Moreover, the interaction of DLK1 with NOTCH1 caused an inhibition of basal NOTCH signaling in preadipocytes and mesenchymal multipotent cells. In this work, we demonstrate, for the first time, that DLK2 interacts with itself, with DLK1, and with the same NOTCH1 receptor region as DLK1 does. We demonstrate also that the interaction of DLK2 with NOTCH1 similarly results in an inhibition of NOTCH signaling in preadipocytes and Mouse Embryo fibloblasts. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | NOTCH Signaling, NOTCH Signaling and Myogenesis |
| + |
MDM2 | up-regulates
ubiquitination
|
NOTCH1 |
0.479 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-200197 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23252402 |
Although the interaction between notch1 and mdm2 results in ubiquitination of notch1, this does not result in degradation of notch1, but instead leads to activation of the intracellular domain of notch1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD signaling |
| + |
DLL3 | up-regulates activity
binding
|
NOTCH1 |
0.488 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-209738 |
|
|
Homo sapiens |
B-lymphocyte |
| pmid |
sentence |
| 16140393 |
Notch signaling is a highly conserved pathway involved in cell fate choice during development with Delta and Jagged constituting the two evolutionary conserved families of Notch ligands. These ligands are transmembrane proteins with conserved biochemical structure that share their receptors and signal through a common mechanism. Upon ligand binding Notch receptors are proteoliticaly cleaved, the intracellular domain of Notch (NICD) is released and translocated to the nucleus, where it activates target genes. In mammals, four receptors and five ligands have been described. Delta-1, Delta-3 and Delta-4 are homologues to Drosophila Delta and Jagged-1 and Jagged-2 to Drosophila Serrate. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | NOTCH Signaling |
| + |
CDK8 | down-regulates
phosphorylation
|
NOTCH1 |
0.55 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-130640 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15546612 |
Purified recombinant cycc:cdk8 phosphorylates the notch icd within the tad and pest domains, and expression of cycc:cdk8 strongly enhances notch icd hyperphosphorylation and pest-dependent degradation by the fbw7/sel10 ubiquitin ligase in vivo. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DLL4 | up-regulates activity
binding
|
NOTCH1 |
0.641 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-209735 |
|
|
Homo sapiens |
B-lymphocyte |
| pmid |
sentence |
| 16140393 |
Notch signaling is a highly conserved pathway involved in cell fate choice during development with Delta and Jagged constituting the two evolutionary conserved families of Notch ligands. These ligands are transmembrane proteins with conserved biochemical structure that share their receptors and signal through a common mechanism. Upon ligand binding Notch receptors are proteoliticaly cleaved, the intracellular domain of Notch (NICD) is released and translocated to the nucleus, where it activates target genes. In mammals, four receptors and five ligands have been described. Delta-1, Delta-3 and Delta-4 are homologues to Drosophila Delta and Jagged-1 and Jagged-2 to Drosophila Serrate. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-77973 |
|
|
Homo sapiens |
Hematopoietic Cell |
| pmid |
sentence |
| 10837024 |
Expression analysis of known notch ligands suggests that dll4 is the only ligand that exhibits spatial and temporal expression consistent with the activation of notch1 and notch4 during vascular development. The identification of dll4 reveals a candidate ligand for notch receptors involved in blood vessel biology |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-112649 |
|
|
Homo sapiens |
Hematopoietic Cell |
| pmid |
sentence |
| 11739188 |
Expression analysis of known notch ligands suggests that dll4 is the only ligand that exhibits spatial and temporal expression consistent with the activation of notch1 and notch4 during vascular development. The identification of dll4 reveals a candidate ligand for notch receptors involved in blood vessel biology |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| Pathways: | NOTCH Signaling |
| + |
NOTCH1 | up-regulates activity
binding
|
ZMIZ1 |
0.454 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263937 |
|
|
Mus musculus |
T-cell Lymphoma Cell |
| pmid |
sentence |
| 26522984 |
The N-terminal domain (NTD) is critical for Zmiz1 to function as a Notch collaborator. Zmiz1 and Notch1 cooperatively recruit each other to chromatin through the TPR domain. The N-terminal domain (NTD) of Zmiz1 is important for enhancing Notch reporter activity and contains tetratricopeptide repeats (TPR) that mediate protein-protein interactions |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
RUNX3 | down-regulates
binding
|
NOTCH1 |
0.688 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-188338 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19800882 |
To investigate the possible mechanism of the down-regulation of hes-1 by runx3, we performed western blot and reporter assay and found that runx3 suppressed intracellular domain of notch1 (icn1)-mediated transactivation of notch signaling while it did not alter the expression of icn1 and recombination signal binding protein-j kappa (rbp-j) in smmc7721 cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOTCH1 | up-regulates activity
relocalization
|
HIF1A |
0.647 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-141315 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 16256737 |
The notch intracellular domain interacts with hif-1alpha and hif-1alpha is recruited to notch-responsive promoters upon notch activation under hypoxic conditions. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | NOTCH Signaling |
| + |
DAB1 | up-regulates
binding
|
NOTCH1 |
0.381 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-196438 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22394407 |
The induction of disabled-1 (dab-1) tyrosine phosphorylation, and the subsequent activation of src family kinases, were found to be essential steps for the activation of notch-1 signaling by reelin |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Brain |
| + |
ADAM17 | up-regulates activity
cleavage
|
NOTCH1 |
0.738 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-78903 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10882063 |
... here we show that an additional processing event occurs in the extracellular part of the receptor, preceding cleavage by the gamma-secretase-like activity. Purification of the activity accounting for this cleavage in vitro shows that it is due to tace (tnfalpha-converting enzyme), a member of the adam (a disintegrin and metalloprotease domain) family of metalloproteases. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | NOTCH Signaling, NOTCH Signaling and Myogenesis |
| + |
CCND1 | up-regulates
|
NOTCH1 |
0.638 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-165189 |
|
|
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 20443831 |
The mechanism by which cyclin d1 enhances notch1 activity in different cell types remains to be determined;the current studies demonstrate for the first time that notch1 activity is induced by cyclin d1. The expression of cyclin d1 sirna reduced notch1 activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Breast |
| Pathways: | Acute Myeloid Leukemia |
| + |
RERE | up-regulates activity
binding
|
NOTCH1 |
0.319 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264486 |
|
|
Homo sapiens |
Neuroblastoma Cell Line |
| pmid |
sentence |
| 28144959 |
In mammalian cells, RERE co‐immunoprecipitates with CBF1 and Notch intracellular domain (NICD), and is recruited to nuclear foci formed by over‐expressed NICD1. RERE is also necessary for NICD to activate the expression of Notch target genes. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOTCH1 | down-regulates
binding
|
TCF3 |
0.43 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-56150 |
|
|
Homo sapiens |
B-lymphocyte |
| pmid |
sentence |
| 9528794 |
We provide evidence that notch and deltex may act on e47 by inhibiting signaling through ras because (i) full e47 activity was found to be dependent on ras and (ii) both notch and deltex inhibited gal4-jun, a hybrid transcription factor whose activity is dependent on signaling from ras to sapk/jnk. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GSK3A | down-regulates
phosphorylation
|
NOTCH1 |
0.321 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-183969 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19214430 |
Taken together, our results indicate that gsk-3alfa is a negative regulator of notch1/nicd. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOTCH1 | up-regulates
binding
|
SNW1 |
0.599 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-86125 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11404076 |
Contact with skip is required for biological activity of notchic. A mutation in the fourth ankyrin repeat that abolished notch signal transduction did not affect interaction with cbf1 but abolished interaction with skip. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-75782 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10713164 |
SKIP, a CBF1-associated protein, interacts with the ankyrin repeat domain of NotchIC To facilitate NotchIC function. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
KPNA3 | up-regulates
relocalization
|
NOTCH1 |
0.325 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-165280 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20454918 |
Nicd binds via one of its four potential nuclear localization signals to importins alfa3, alfa4, and alfa7. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIN1 | up-regulates
binding
|
NOTCH1 |
0.386 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-183461 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19151708 |
Prolyl-isomerase pin1 interacts with notch1 and affects notch1 activation. Pin1 potentiates notch1 cleavage by gamma-secretase, leading to an increased release of the active intracellular domain and ultimately enhancing notch1. pin1 potentiates notch1 cleavage by gamma-secretase |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
BCL2 |
0.264 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-149730 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 16990763 |
Other notch target genes identi__ed in the thymoma cell line were dtx1 (gene for deltex1), i__-202, i__-204, i__-d3, adam19 (meltrinb).24 a number of other genes have been reported as being notch targets, including notch1 itself,28 nrarp in xenopus embryos,29 bcl2 in thymoma cells,30 ccnd1 (gene for cyclin d1) in a kidney cell line,31 dkn1a (gene for cyclindependent kinase inhibitor 1a (p21, cip1)) in keratinocytes32 and tcf3 (gene for e2a). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD signaling |
| + |
MAML1 | up-regulates quantity by expression
transcriptional regulation
|
NOTCH1 |
0.923 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-94029 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12370315 |
It has been shown that maml1 binds directly to the ankyrin repeat region of notch1 and forms a dna-binding complex with icn and csl |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAML1 | up-regulates
binding
|
NOTCH1 |
0.923 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-84827 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11101851 |
Maml1 binds to the ankyrin repeat domain of all four mammalian notch receptors, forms a dna-binding complex with icn and rbp-jkappa, and amplifies notch-induced transcription of hes1. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-86117 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11390662 |
Maml1 binds to the ankyrin repeat domain of all four mammalian notch receptors, forms a dna-binding complex with icn and rbp-jkappa, and amplifies notch-induced transcription of hes1.Maml1 functions as a transcriptional co-activator for notch signalling. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
PSEN1 | up-regulates
cleavage
|
NOTCH1 |
0.797 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-72886 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10593990 |
Presenilin-1 (ps1), a polytopic membrane protein primarily localized to the endoplasmic reticulum, is required for efficient proteolysis of both notch and beta-amyloid precursor protein (app) within their trans- membrane domains. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CTNNB1 | up-regulates
binding
|
NOTCH1 |
0.774 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236858 |
|
|
Mus musculus |
C2C12 Cell |
| pmid |
sentence |
| 19000719 |
Beta-catenin can regulate the level and transcriptional activity of the notch1 and notch1 intracellular domain (nicd). The in vivo and in vitro results demonstrate that beta-catenin binds with notch1 and nicd, for which its armadillo repeat domain is essential. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, FLT3-ITD signaling, Retinoic acid Signaling |
| + |
FBXW7 | down-regulates quantity by destabilization
ubiquitination
|
NOTCH1 |
0.618 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-130706 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15546612 |
Purified recombinant cycc:cdk8 phosphorylates the notch icd within the tad and pest domains, and expression of cycc:cdk8 strongly enhances notch icd hyperphosphorylation and pest-dependent degradation by the fbw7/sel10 ubiquitin ligase in vivo. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
FOXO | down-regulates quantity 
transcriptional regulation
|
NOTCH1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252940 |
|
|
Mus musculus |
Satellite Cell |
| pmid |
sentence |
| 24749067 |
We demonstrate that FOXO3, perhaps by activating Notch signaling, promotes the quiescent state during SC self-renewal in adult muscle regeneration. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, FLT3-ITD signaling |
| + |
GXYLT1 | up-regulates
glycosylation
|
NOTCH1 |
0.385 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-177691 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22117070 |
Activity on notch egf repeats was proven by in vitro xylosylation of a mouse notch1 fragment recombinantly produced in sf9 insect cells, a bacterially expressed egf repeat from mouse notch2 modified in vitro by rumi and gxylt2 and in vivo by co-expression of the enzyme with the notch1 fragment. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CSK | up-regulates
binding
|
NOTCH1 |
0.282 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-196824 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22479394 |
We found that the notch-1-furin interaction is regulated by the non-receptor tyrosine kinase, c-src. c-src and notch-1 are physically associated, and this association is responsible for notch-1 processing and activation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
XXYLT1 | up-regulates
binding
|
NOTCH1 |
0.315 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-177745 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22117070 |
Xxylt1 acts on the xyl1,3glc-o-linked glycan of notch egf domains. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOTCH1 | up-regulates
|
BMPR1A/1B/2 |
0.356 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-114592 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22298955 |
Similar synergy is found in notch and bmp crosstalk: activating notch signaling enhanced bmp-induced alp activity and formation of calcified nodules in vitro. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOTCH1 | up-regulates
binding
|
RBPJ |
0.95 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-183510 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19165418 |
The intracellular part of the notch receptor is cleaved off and translocates to the nucleus, where it binds to the transcription factor rbp-j. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CNTN6 | up-regulates
relocalization
|
NOTCH1 |
0.586 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-124151 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 15082708 |
Here, we establish that nb-3, a member of the f3/contactin family, acts as a novel notch ligand to participate in oligodendrocyte generation. Nb-3 triggers nuclear translocation of the notch intracellular domain and promotes oligodendrogliogenesis from progenitor cells and differentiation of oligodendrocyte precursor cells via deltex1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RUNX2 | down-regulates
binding
|
NOTCH1 |
0.384 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-167627 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20740684 |
Runx2 is an inhibitor of the notch1 signaling pathway during normal osteoblast differentiation. The n-terminal domain of runx2 was crucial to the binding and inhibition of the the n-terminus of the notch1 intracellular domain. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
gamma-secretase | up-regulates activity
cleavage
|
NOTCH1 |
0.677 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-209717 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25610395 |
The membrane-bound Notch segment that results from this cleavage, known as Notch Intracellular Truncation domain (NEXT), is a γ-secretase substrate. γ-Secretase performs the subsequent cleavage at S3, releasing Notch intracellular domain (NICD) from the membrane and allowing for signal transduction through binding with the CBL-1, Su(H), Lag-1 family of DNA binding proteins. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | NOTCH Signaling, NOTCH Signaling and Myogenesis |
| + |
SDC3 | up-regulates activity
binding
|
NOTCH1 |
0.382 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-244072 |
|
|
Mus musculus |
Satellite Cell |
| pmid |
sentence |
| 20696709 |
Furthermore, we show that Syndecan-3 interacts with Notch and is required for Notch processing by ADAM17/tumor necrosis factor-converting enzyme (TACE) and signal transduction. Together, our data support the conclusion that Syndecan-3 and Notch cooperate in regulating homeostasis of the satellite cell population and myofiber size. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
SNW1 | up-regulates
binding
|
NOTCH1 |
0.599 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-75788 |
|
|
Homo sapiens |
Myoblast |
| pmid |
sentence |
| 10713164 |
Contact with skip is required for biological activity of notchic. A mutation in the fourth ankyrin repeat that abolished notch signal transduction did not affect interaction with cbf1 but abolished interaction with skip. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-108499 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11404076 |
We find that Notch 3 IC, like Notch 1 IC, can bind the SKIP and PCAF proteins |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Tissue: |
Muscle |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
NOTCH1 | down-regulates
|
Neurogenesis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-265769 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 9601631 |
Signalling through activated Notch is known both to control multiple cell fate determinations (in both invertebrates and vertebrates) and to inhibit developmental processes, such as neurogenesis |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Retinoic acid Signaling, Rett syndrome |
| + |
ADAM10 | up-regulates activity
cleavage
|
NOTCH1 |
0.781 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259838 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 28624438 |
ADAM10-mediated Notch1 cleavage is the rate limiting-step for release of the NICD and subsequent activation of Notch1 signaling. In T cells ADAM10-mediated Notch1 shedding controls T cell development |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
LFNG | up-regulates
glycosylation, binding
|
NOTCH1 |
0.756 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-96540 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12486116 |
We demonstrate that egf 12, a portion of the ligand-binding site, is modified with o-fucose and that this site is evolutionarily conserved. We also show that endogenous fringe proteins in chinese hamster ovary cells (lunatic fringe and radical fringe) as well as exogenous manic fringe modify o-fucose on many but not all egf repeats of mouse notch1. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-96537 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12486116 |
We demonstrate that egf 12, a portion of the ligand-binding site, is modified with o-fucose and that this site is evolutionarily conserved. We also show that endogenous fringe proteins in chinese hamster ovary cells (lunatic fringe and radical fringe) as well as exogenous manic fringe modify o-fucose on many but not all egf repeats of mouse notch1. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Tissue: |
Ovary |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
PIN1 |
0.386 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-183458 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19151708 |
Notch1 directly induces transcription of pin1 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DNER | up-regulates
binding
|
NOTCH1 |
0.459 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-138346 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 15965470 |
Dner binds to notch1 at cell-cell contacts and activates notch signaling in vitro. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
POGLUT1 | up-regulates
glycosylation
|
NOTCH1 |
0.605 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-198713 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22872643 |
O-glucosylation of epidermal growth factor-like (egf) repeats in the extracellular domain of notch is essential for notch function. A udp-glucose:protein o-glucosyltransferase (poglut/rumi) transfers o-glucose to serine within the o-glucose consensus. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
NFKB1 |
0.378 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-110963 |
|
|
Homo sapiens |
B-lymphocyte |
| pmid |
sentence |
| 11591772 |
Nf-kappab activity is regulated by notch-1 via transcriptional control of nf-kappab. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | NOTCH Signaling |
| + |
NLK | down-regulates
phosphorylation
|
NOTCH1 |
0.384 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163697 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20118921 |
Nlk-phosphorylated notch1icd is impaired in its ability to form a transcriptionally_ active_ ternary_ complex. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GXYLT2 | up-regulates
binding
|
NOTCH1 |
0.385 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-177714 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22117070 |
Recently, we have shown (28) that two members of the human glycosyltransferase 8 family (gt8) (29), gxylt1 and gxylt2 (glucoside-xylosyltransferase 1/2), are able to transfer the first alfa1,3-linked xylose to o-glucosylated mammalian notch egf repeats. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SMAD3 | up-regulates
binding
|
NOTCH1 |
0.547 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-119374 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14638857 |
Nicd and smad3 were shown to interact directly, both in vitro and in cells, in a ligand-dependent manner, and smad3 could be recruited to csl-binding sites on dna in the presence of csl and nicd |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOTCH1 | up-regulates quantity by expression
|
PAX7 |
0.394 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-219374 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22493066 |
Constitutive Notch Activation Upregulates Pax7 and Promotes the Self-Renewal of Skeletal Muscle Satellite Cells |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Skeletal Muscle, Satellite Cell |
| Pathways: | Acute Myeloid Leukemia, NOTCH Signaling and Myogenesis |
| + |
RFNG | up-regulates
binding
|
NOTCH1 |
0.646 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-96561 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12486116 |
We demonstrate that egf 12, a portion of the ligand-binding site, is modified with o-fucose and that this site is evolutionarily conserved. We also show that endogenous fringe proteins in chinese hamster ovary cells (lunatic fringe and radical fringe) as well as exogenous manic fringe modify o-fucose on many but not all egf repeats of mouse notch1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Ovary |
| + |
FURIN | up-regulates
binding
|
NOTCH1 |
0.665 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-196914 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22479394 |
The proteolytic activity of furin responsible for processing full length notch-1 (p300) plays a critical role in notch signaling. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
HOXA5 |
0.318 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-149770 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 16990763 |
Other than a role in t-cell development, the hox genes may be involved in alternative notchregulated processes in hematopoietic stem cells. Notch signaling is clearly important for self-renewal of hematopoietic progenitors (reviewed by radkte et al. 57). Interestingly, hoxa5, a9 and a10 were found to be part of the stem cell profile' |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NBEA | down-regulates activity
binding
|
NOTCH1 |
0.306 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266010 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 26999814 |
Yeast two-hybrid identified the Notch1 intracellular domain as a physical interactor of the PBW domain and a role for NBEA as a negative regulator in Notch-mediated transcription was demonstrated.|Defining novel interaction partners of conserved NBEA domain modules identified a role for NBEA as transcriptional regulator in the nucleus. The physical interaction of NBEA with NOTCH1 is most relevant for ASD pathogenesis because NOTCH signaling is essential for neural development. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Central Nervous System |
| + |
FOXO3 | down-regulates quantity
transcriptional regulation
|
NOTCH1 |
0.378 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-244076 |
|
|
Mus musculus |
Satellite Cell |
| pmid |
sentence |
| 24749067 |
We demonstrate that FOXO3, perhaps by activating Notch signaling, promotes the quiescent state during SC self-renewal in adult muscle regeneration. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
ZMIZ1 | up-regulates activity
binding
|
NOTCH1 |
0.454 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263936 |
|
|
Mus musculus |
T-cell Lymphoma Cell |
| pmid |
sentence |
| 26522984 |
The N-terminal domain (NTD) is critical for Zmiz1 to function as a Notch collaborator. Zmiz1 and Notch1 cooperatively recruit each other to chromatin through the TPR domain. The N-terminal domain (NTD) of Zmiz1 is important for enhancing Notch reporter activity and contains tetratricopeptide repeats (TPR) that mediate protein-protein interactions |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
NUMB | down-regulates quantity by destabilization
ubiquitination
|
NOTCH1 |
0.798 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-99762 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 12682059 |
Mammalian numb proteins promote notch1 receptor ubiquitination and degradation of the notch1 intracellular domain |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | NOTCH Signaling and Myogenesis |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
NFKB2 |
0.289 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-56097 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9528780 |
In transient-transfection assays we show that truncated notch-1 strongly induces nf-kappab2 promoter activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
POFUT1 | up-regulates
binding
|
NOTCH1 |
0.745 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-104627 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12909620 |
Notch_ is modified in its epidermal growth factor-like domains by the addition of_ fucose_ to serine or threonine residues. O-fucosylation is mediated by protein o-fucosyltransferase 1 and down-regulation of this enzyme by rna interference or mutation of the ofut1 gene in drosophila or by mutation of the pofut1 gene in mouse prevents notch signaling. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
HES1 |
0.772 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-183507 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19165418 |
Several lines of evidence have suggested that these genes are indeed direct notch target genes: a) the promoters of hes1, hes5 and hes7 as well as hey1, hey2 and heyl subfamily of hes, related with yrpw motif) can be activated by a constitutive active form of notch1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, NOTCH Signaling, NOTCH Signaling and Myogenesis, Retinoic acid Signaling |
| + |
NOTCH1 | up-regulates
|
Differentiation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-241998 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18342499 |
Genetic ablation or activation of the pathway reveals that Notch signalling promotes differentiation of the hair follicle, sebaceous gland and interfollicular epidermal lineages |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, NOTCH Signaling |
| + |
NOTCH1 | form complex 
binding
|
RBPJ/NOTCH |
0.95 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254381 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 7566092 |
Here we show that activated forms of mNotch associate with the human analogue of Su(H), KBF2/RBP-Jk and act as transcriptional activators through the KBF2-binding sites of the HES-1 promoter. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | NOTCH Signaling, NOTCH Signaling and Myogenesis, Retinoic acid Signaling |
| + |
MECP2 | down-regulates quantity by repression
transcriptional regulation
|
NOTCH1 |
0.292 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264675 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 25420914 |
As the first step to reveal how MeCP2 phosphorylation may regulate Notch signaling, we conducted chromatin immunoprecipitation (ChIP) experiment to determine whether the phosphor-mutant MeCP2 protein has altered promoter occupancy at the promoters of Dll1 and Notch1. We found increased binding of the phosphor-mutant protein at the promoters of both Dll1 and Notch1 |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, Rett syndrome |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
ERBB2 |
0.5 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-145322 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 16554461 |
Notch1 activation by neuronal contact induces the glial expression of the brain lipid binding protein (blbp) and erbb2 genes. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
HEYL |
0.609 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-83399 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11044625 |
These data confirm heyl as a notch1 target gene that is likely involved in somite formation and patterning. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Muscle, Smooth Muscle |
| + |
LCK | up-regulates
binding
|
NOTCH1 |
0.459 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-118902 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 14583609 |
Endogenous notch-1 associates with p56(lck) and pi3k. p56(lck) is required for the notch-1-mediated activation of akt/pkb function |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
TCF12 |
0.368 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-197514 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22577461 |
E2a positively regulates notch1 expression, which induces the expression of hebalt, bcl11b, and il7r. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GSK3B | up-regulates
phosphorylation
|
NOTCH1 |
0.466 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-90608 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12123574 |
Here, we observed that gsk3beta was able to bind and phosphorylate notch1ic in vitro, and attenuation of gsk3beta activity reduced phosphorylation of notchic in vivo.Functionally, ligand-activated signaling through the endogenous notch1 receptor was reduced in gsk3beta fibroblasts, implying a positive role for gsk3beta in mammalian notch signaling. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD signaling |
| + |
NOTCH1 | up-regulates quantity by expression
transcriptional regulation
|
TCFL5 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-149807 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 16990763 |
Interestingly, in absence of delta signal, both hes-1 and tcfl5 decreased, and further decreased by incubation with dapt. (figure 4). This pharmacological approach therefore provides additional evidence that tcfl5, similar to hes1, is a true notch target gene. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
NOTCH1
- 
- 