| + |
SMAD3 | up-regulates quantity by expression 
transcriptional regulation
|
CDKN2B |
0.544 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-245441 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 23032366 |
PD-1 inhibits T cell proliferation by upregulating p27 and p15 and suppressing Cdc25A. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Cell cycle: G1/S phase transition, Pancreatic ductal adenocarcinoma (PDA), TGF-beta Signaling, TGFb in cancer |
| + |
DNMT3A | down-regulates quantity by repression 
transcriptional regulation
|
CDKN2B |
0.36 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261509 |
|
|
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 |
| + |
CDKN2B | down-regulates
|
Proliferation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259407 |
|
|
Mus musculus |
Myeloid Leukemia Cell |
| pmid |
sentence |
| 14681685 |
The Ink4b gene (Cdkn2b) encodes p15Ink4b, a cyclin-dependent kinase inhibitor. It has been implicated in playing a role in the development of acute myeloid leukemia (AML) in man, since it is hypermethylated with high frequency. We provide evidence that the gene is a tumor suppressor for myeloid leukemia in mice. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Pancreatic ductal adenocarcinoma (PDA), TGF-beta Signaling, TGFb in cancer |
| + |
TGFB1 | up-regulates quantity by expression
transcriptional regulation
|
CDKN2B |
0.288 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-29582 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 7592908 |
The steadystate level of p15ink4b mrna was induced 30-fold upon tgf-beta treatment, implicating p15ink4b as a primary effector of the tgf-beta-mediated cell cycle arrest |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Cell cycle: G1/S phase transition, TGF-beta Signaling, TGFb in cancer |
| + |
SMAD2/SMAD4 | up-regulates quantity by expression
transcriptional regulation
|
CDKN2B |
0.586 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256287 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11013220 |
Our data demonstrate the physical interactions and functional cooperativity of Sp1 with a complex of Smad2, Smad3 and Smad4 in the induction of the p15Ink4B gene. These findings explain the tumor suppressor roles of Smad2 and Smad4 in growth arrest signaling by TGF-β. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Pancreatic ductal adenocarcinoma (PDA), TGF-beta Signaling, TGFb in cancer |
| + |
FUBP1 | down-regulates quantity by repression
transcriptional regulation
|
CDKN2B |
0.261 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259126 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19637194 |
The cell cycle inhibitor p15 was also up-regulated upon FBP1 knockdown. Our analysis of HCC cells after FBP1 knockdown suggests that p15 mRNA levels may also (directly or indirectly) depend on FBP1 activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BAP1 | up-regulates quantity by expression 
transcriptional regulation
|
CDKN2B |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-241656 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 26470845 |
Since we found that ASXL1 and BAP1 both are enriched at the INK4B locus, our results suggest that activation of the INK4B locus requires ASXL1/BAP1-mediated deubiquitinylation of H2AK119ub1. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
CDKN2B | down-regulates 
binding
|
CDK4 |
0.874 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-46758 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9042862 |
We present evidence that the different subcellular location of p15 and p27 ensures the prior access of p15 to cdk4. In the cell, p15 is localized mostly in the cytoplasm, whereas p27 is nuclear. p15 prevails over p27 or a p27 construct consisting of the cdk inhibitory domain tagged with a nuclear localization signal. However, when p15 and p27 are forced to reside in the same subcellular location, either the cytoplasm or the nucleus, p15 no longer prevents p27 from binding to cdk4. These properties allow p15 and p27 to coordinately inhibit cdk4 and cdk2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Lung |
| Pathways: | Pancreatic ductal adenocarcinoma (PDA) |
| + |
SP1 | up-regulates quantity by expression
transcriptional regulation
|
CDKN2B |
0.538 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256289 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11013220 |
In this system, the basal transcription level from the p15Ink4B promoter was increased with increasing levels of Sp1, and Sp1 was required for transcriptional induction by Smads. Finally, inactivation of the Sp1 binding sites in the p15Ink4B promoter decreased the basal transcription level and TGF-β responsiveness. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SMAD3/SMAD4 | up-regulates quantity by expression
transcriptional regulation
|
CDKN2B |
0.587 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256286 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11013220 |
Our data demonstrate the physical interactions and functional cooperativity of Sp1 with a complex of Smad2, Smad3 and Smad4 in the induction of the p15Ink4B gene. These findings explain the tumor suppressor roles of Smad2 and Smad4 in growth arrest signaling by TGF-β. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Pancreatic ductal adenocarcinoma (PDA), TGF-beta Signaling, TGFb in cancer |
| + |
ASXL1 | up-regulates quantity by expression
transcriptional regulation
|
CDKN2B |
0.283 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-241759 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 26470845 |
Tumor suppressor ASXL1 is essential for the activation of INK4B expression in response to oncogene activity and anti-proliferative signals |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
CDKL1 | up-regulates activity
phosphorylation
|
CDKN2B |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273862 |
|
|
Homo sapiens |
Colorectal Cancer Cell Line |
| pmid |
sentence |
| 28352193 |
We demonstrated that depletion of CDKL1 notably upregulated the protein expression of P15. P15 is shown to be a target of CDKL1 in CRC, either direct or indirect. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MYC | down-regulates quantity by repression
transcriptional regulation
|
CDKN2B |
0.588 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-102746 |
|
|
Homo sapiens |
Leukemia Cell |
| pmid |
sentence |
| 12835716 |
Miz1 is a zinc finger transcription factor with an n-terminal poz domain. Complexes with myc, bcl-6 or gfi-1 repress expression of genes like cdkn2b (p15(ink4)) or cdkn1a (p21(cip1)). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Cell cycle: G1/S phase transition |
| + |
SWI/SNF complex | up-regulates quantity by expression
transcriptional regulation
|
CDKN2B |
0.295 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256300 |
|
|
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 |
| + |
FOXO1 | up-regulates quantity by expression
transcriptional regulation
|
CDKN2B |
0.31 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-157794 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17873901 |
Foxo1a strongly activated p15ink4b transcription and p19ink4d transcription, while foxo3a showed higher p19ink4d transcription activity than p15ink4b transcription activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ZNF304 | down-regulates quantity by repression
transcriptional regulation
|
CDKN2B |
0.285 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266099 |
|
|
Homo sapiens |
DLD-1 Cell |
| pmid |
sentence |
| 24623306 |
Finally, we show that ZNF304 also directs transcriptional silencing of INK4-ARF in human embryonic stem cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FOXO | up-regulates quantity by expression
transcriptional regulation
|
CDKN2B |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252917 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17873901 |
Foxo1a strongly activated p15ink4b transcription and p19ink4d transcription, while foxo3a showed higher p19ink4d transcription activity than p15ink4b transcription activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
CDKN2B
- 
- 