| + |
IKBKB | down-regulates 
phosphorylation
|
CDKN2A |
0.405 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163801 |
Ser8 |
MEPAAGSsMEPSADW |
Homo sapiens |
|
| pmid |
sentence |
| 20152798 |
Ikkbeta specifically binds to p16 and phosphorylates ser8 of p16 phosphorylation at ser8 of p16 brings about a significant loss of its cyclin-dependent kinase (cdk) 4-inhibitory activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MYC | down-regulates quantity by repression
transcriptional regulation
|
CDKN2A |
0.758 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-102743 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12835716 |
C-myc also directly represses transcription of cdk kinase inhibitors including p27kip1, p21cip1, p15ink4b and p16ink4a |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, DNMT3A in AML, NPM1 in AML, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, Triple mutant AML, NPM1_new, Rhabdomyosarcoma |
| + |
CDKN2A | down-regulates 
|
Proliferation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259406 |
|
|
Homo sapiens |
Carcinoma Cell |
| pmid |
sentence |
| 7972006 |
Transfection of the p16INK4 cDNA expression vector into carcinoma cells inhibits their colony-forming efficiency and the p16INK4 expressing cells are selected against with continued passage in vitro. These results are consistent with the hypothesis that p16INK4 is a tumor-suppressor protein and that genetic and epigenetic abnormalities in genes controlling the G1 checkpoint can lead to both escape from senescence and cancer formation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, ASXL1 in AML, DNMT3A in AML, Onco-fusion proteins in AML, NPM1 in AML, Luminal Breast Cancer, Malignant Melanoma, Triple mutant AML, NPM1_new, Pancreatic ductal adenocarcinoma (PDA), Rhabdomyosarcoma, TGFb in cancer |
| + |
CDKN2A | down-regulates activity
binding
|
CyclinD/CDK4 |
0.822 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217514 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8891723 |
The first group, including p16ink4a, p15ink4b,p18ink4cand p19ink4d, is specific for the g1 cdks,cdk4and cdk6, inhibiting the kinase activity of cyclin d/cdk4-cdk6 complexes on prb. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-245459 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11154267 |
Overexpression of p16INK4a in cells with functional pRb results in inhibition of both Cdk4- and Cdk6-associated kinase activity and pRb phosphorylation, with subsequent cell cycle arrest (46, 50). In addition, inhibition of D cyclin-Cdk4 complex formation by p16INK4a prevents sequestration of p21Cip1 and p27Kip1 by these complexes in early G1, leading to suppression of cyclin E-Cdk2 activity |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, Luminal Breast Cancer, Malignant Melanoma, Pancreatic ductal adenocarcinoma (PDA), Rhabdomyosarcoma |
| + |
MYC | down-regulates quantity by repression
transcriptional regulation
|
CDKN2A |
0.758 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267575 |
|
|
Homo sapiens |
Lymphoma Cell |
| pmid |
sentence |
| 20551174 |
In tissue culture, ectopic expression of Myc suppresses the cell cycle arrest that occurs in response to several anti-mitogenic signals such as transforming growth factor β (TGFβ), since Myc represses expression of the cyclin-dependent kinase inhibitors (CKIs) p15ink4b, p21cip1, and p57kip2 via interaction with Miz1 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, DNMT3A in AML, NPM1 in AML, Cell cycle: G1/S phase transition, Cell cycle: G2/M phase transition, Triple mutant AML, NPM1_new, Rhabdomyosarcoma |
| + |
NDN | up-regulates 
|
CDKN2A |
0.282 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253383 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24392140 |
In HEK293A cells transfected with luciferase reporter constructs, necdin relieves Bmi1-dependent repression of p16 promoter activity, |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
POMC | up-regulates quantity by expression
transcriptional regulation
|
CDKN2A |
0.27 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252377 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11830546 |
The expression of the melanoma susceptibility gene product p16 is increased after UVR both in epidermally derived cell lines and in human skin. the increased expression of p16 after exposure to suberythemal doses of UVR is potentiated by α-MSH, a ligand for MC1R, and this effect is mimicked by cAMP, the intracellular mediator of α-MSH signaling via the MC1 receptor. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CDKN2A | down-regulates
binding
|
CDK6 |
0.866 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-44557 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8891723 |
The first group, including p16ink4a, p15ink4b,p18ink4cand p19ink4d, is specific for the g1 cdks,cdk4and cdk6, inhibiting the kinase activity of cyclin d/cdk4-cdk6 complexes on prb. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-140412 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16161044 |
In addition, cytoplasmic p16 bound cyclin dependent kinase (cdk)4/6, potentially indicating that p16 could have a function in the cytoplasm. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML |
| + |
CDKN2A | down-regulates
binding
|
CDK4 |
0.902 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-44554 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8891723 |
The first group, including p16ink4a, p15ink4b,p18ink4cand p19ink4d, is specific for the g1 cdks, cdk4 and cdk6, inhibiting the kinase activity of cyclin d/cdk4-cdk6 complexes on prb. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-140409 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16161044 |
The cdk-inhibitor p16 is a tumor suppressor gene that is inactivated in many forms of cancer. In addition, cytoplasmic p16 bound cyclin dependent kinase (cdk)4/6, potentially indicating that p16 could have a function in the cytoplasm. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Pancreatic ductal adenocarcinoma (PDA) |
| + |
CTBP1 | down-regulates quantity by repression
transcriptional regulation
|
CDKN2A |
0.423 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259195 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23303449 |
Our findings suggest an important role of CtBP1 in the transcriptional control of p16INK4a and Brca1[.]. Additionally, the inhibitor of cyclin-dependent protein kinases (CDKs), p16INK4a, whose loss has been related to the pathogenesis of melanoma, was repressed by CtBP1 as well. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, ASXL1 in AML |
| + |
DNMT3A | down-regulates quantity by repression
transcriptional regulation
|
CDKN2A |
0.388 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255809 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26350239 |
Quantitative real-time PCR (qPCR) was used to investigate the effect of DNMT3A on p18INK4C expression, along with the other INK4 members, including p15INK4B, p16INK4A and p19INK4D. The results showed that the depletion of DNMT3A increased the transcriptional levels of the four members of the INK4 family |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, Onco-fusion proteins in AML, Triple mutant AML |
| + |
Polycomb repressive complex 2 | down-regulates quantity by repression
transcriptional regulation
|
CDKN2A |
0.345 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256122 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22469984 |
The requirement for PRC2 in leukemia is partly because of its role in direct transcriptional repression of genes that limit the self-renewal potential of hematopoietic cells, including Cdkn2a |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SWI/SNF complex | up-regulates quantity by expression
transcriptional regulation
|
CDKN2A |
0.359 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256299 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18332116 |
HSNF5 reexpression in MRT cells caused SWI/SNF recruitment and activation of p15INK4b and p16INK4a, but not of p14ARF.Reexpression of hSNF5 in MRT cells overcomes epigenetic silencing and mediates transcriptional activation of p15INK4b and p16INK4a |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BMI1 | down-regulates quantity by repression
transcriptional regulation
|
CDKN2A |
0.47 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253385 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24392140 |
In HEK293A cells transfected with luciferase reporter constructs, necdin relieves Bmi1-dependent repression of p16 promoter activity, |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CDKN2A | down-regulates
binding
|
CDK2 |
0.494 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-64431 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10022885 |
However, induction of p16(ink4a) also causes marked inhibition of cdk2 activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CDKN2A | down-regulates
binding
|
CyclinD1/CDK6 |
0.803 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259810 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8891723 |
The first group, including p16ink4a, p15ink4b,p18ink4cand p19ink4d, is specific for the g1 cdks,cdk4and cdk6, inhibiting the kinase activity of cyclin d/cdk4-cdk6 complexes on prb. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Pancreatic ductal adenocarcinoma (PDA) |
| + |
CDKN2A | down-regulates
|
Immortality |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259286 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10648628 |
Human keratinocytes that express hTERT and also bypass a p16(INK4a)-enforced mechanism that limits life span become immortal yet retain normal growth and differentiation characteristics |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Pancreatic ductal adenocarcinoma (PDA) |
| + |
BMI1 | down-regulates quantity by repression
transcriptional regulation
|
CDKN2A |
0.47 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-166163 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20551323 |
One important pathway in which bmi-1 acts to promote the overall growth of mice and cellular proliferation includes cdkn2a;bmi-1 represses the expression of cdkn2a, which encodes two cyclin-dependent kinase inhibitors, p16ink4a (p16) and p19arf |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MEIS2 | up-regulates quantity by expression 
transcriptional regulation
|
CDKN2A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267240 |
|
|
Homo sapiens |
MCF-7 Cell |
| pmid |
sentence |
| 21746878 |
We show that the Pbx1 and Meis2 homeodomain proteins interact with Klf4 and can be recruited to DNA elements comprising a Klf4 site or G C box, with adjacent Meis and Pbx sites. Meis2d and Pbx1a activate expression of p15(Ink4a) and E-cadherin, dependent on the Meis2d transcriptional activation domain. We suggest a model in which genes with Klf4 sites can be cooperatively activated by Meis2/Pbx1 and Klf4, dependent primarily on recruitment by Klf4. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PBX1 | up-regulates quantity by expression
transcriptional regulation
|
CDKN2A |
0.314 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267239 |
|
|
Homo sapiens |
MCF-7 Cell |
| pmid |
sentence |
| 21746878 |
We show that the Pbx1 and Meis2 homeodomain proteins interact with Klf4 and can be recruited to DNA elements comprising a Klf4 site or G C box, with adjacent Meis and Pbx sites. Meis2d and Pbx1a activate expression of p15(Ink4a) and E-cadherin, dependent on the Meis2d transcriptional activation domain. We suggest a model in which genes with Klf4 sites can be cooperatively activated by Meis2/Pbx1 and Klf4, dependent primarily on recruitment by Klf4. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TBX5 | up-regulates quantity by expression
transcriptional regulation
|
CDKN2A |
0.271 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255253 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20802524 |
TBX5 suppressed tumor cell proliferation and metastasis through the upregulation of cyclin-dependent kinase inhibitor 2A, metastasis suppressor 1 and downregulation of synuclein gamma and metastasis-associated protein 1 family member 2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ASXL1 | up-regulates quantity by expression
transcriptional regulation
|
CDKN2A |
0.306 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260119 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 29967380 |
Modeling ASXL1 mutation revealed impaired hematopoiesis caused by derepression of p16Ink4a through aberrant PRC1-mediated histone modification. These results indicated that loss of protein interaction between Asxl1 mutant and Bmi1 affected the activity of PRC1, and subsequent derepression of p16Ink4a by aberrant histone ubiquitination could induce cellular senescence, resulting in low-risk MDS-like phenotypes in Asxl1G643fs/+ mice. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, ASXL1 in AML |
| + |
UV stress | up-regulates
|
CDKN2A |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252376 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11830546 |
The expression of the melanoma susceptibility gene product p16 is increased after UVR both in epidermally derived cell lines and in human skin. The increased expression of p16 after exposure to suberythemal doses of UVR is potentiated by α-MSH, a ligand for MC1R, and this effect is mimicked by cAMP, the intracellular mediator of α-MSH signaling via the MC1 receptor. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Malignant Melanoma |
3.0
CDKN2A
- 
- 