+ |
CyclinC/CDK3 | down-regulates activity
phosphorylation
|
TFCP2 |
0.269 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-273180 |
Ser309 |
SLGEGNGsPNHQPEP |
Homo sapiens |
|
pmid |
sentence |
19237534 |
In vitro, lsf is phosphorylated by cyclin e/cyclin-dependent kinase 2 (cdk2), cyclin c/cdk2, and cyclin c/cdk3, predominantly on s309. Phosphorylation by cyclin c/cyclin-dependent kinase 2 following mitogenic stimulation of murine fibroblasts inhibits transcriptional activity of lsf during g1 progression |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CyclinC/CDK3 | down-regulates activity
phosphorylation
|
RB1 |
0.425 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-273181 |
Ser811 |
IYISPLKsPYKISEG |
Homo sapiens |
|
pmid |
sentence |
15084261 |
The active form of prb is underphosphorylated. Cdk3/cyclin-c-mediated phosphorylation at ser-807 and ser-811 is required for g0-g1 transition. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CCNC | form complex
binding
|
CyclinC/CDK3 |
0.681 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-273156 |
|
|
Homo sapiens |
MOLT-16 Cell |
pmid |
sentence |
25344755 |
Cyclin C was cloned as a growth-promoting G1 cyclin, and was also shown to regulate gene transcription. Here we report that in vivo cyclin C acts as a haploinsufficient tumor suppressor, by controlling Notch1 oncogene levels. Cyclin C activates an “orphan” CDK19 kinase, as well as CDK8 and CDK3. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CyclinC/CDK3 | down-regulates quantity by destabilization
phosphorylation
|
NOTCH1 |
0.352 |
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 |
|
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-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 |
|
Publications: |
3 |
Organism: |
In Vitro |
+ |
CyclinC/CDK3 | up-regulates
|
G0/G1_transition |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-273190 |
|
|
|
|
pmid |
sentence |
37104883 |
Among them, CDK3 is critically important because it triggers the transitions of G0 to G1 and G1 to S phase through binding to cyclin C and cyclin E1, respectively. |
|
Publications: |
1 |
+ |
CDK3 | form complex
binding
|
CyclinC/CDK3 |
0.681 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-273157 |
|
|
Homo sapiens |
MOLT-16 Cell |
pmid |
sentence |
25344755 |
Cyclin C was cloned as a growth-promoting G1 cyclin, and was also shown to regulate gene transcription. Here we report that in vivo cyclin C acts as a haploinsufficient tumor suppressor, by controlling Notch1 oncogene levels. Cyclin C activates an “orphan” CDK19 kinase, as well as CDK8 and CDK3. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |