Gene interactions and pathways from curated databases and text-mining

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CCND1 — CDKN2A

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Bova et al., Clin Cancer Res 1999 (Carcinoma, Squamous Cell...) : Loss of p16INK4A in the presence of cyclin D1 overexpression conferred a significantly worse disease-free ( P = 0.011 ) and overall ( P = 0.002 ) survival at 5 years
Lee et al., Int J Mol Med 2000 (Glioma) : p16/INK4a prevents the association of CDK4 with cyclin D1 , and subsequently inhibits phosphorylation of retinoblastoma tumour suppressor protein ( pRb ), thus preventing exit from the G1 phase
Sugimoto et al., Oncogene 2002 : This mitogen induced cyclin D1-kinase activity was blocked by overexpression of p16(INK4a) and resulted in the inhibition of S phase entry in p21/p27-null MEFs
Guo et al., Mol Cell Biol 2004 : We found that ( i ) p19(Arf) or p53 deficiency led to a significant increase in PI 3-kinase activity, which in turn upregulated RhoA and Rac1 activities ; ( ii ) deletion of p19Arf or p53 led to an increase in cell growth rate that was in part dependent on RhoA, Rac1, and Cdc42 activities ; ( iii ) p19(Arf) or p53 deficiency caused an enhancement of the growth related transcription factor NF-kappa B and cyclin D1 activities that are partly dependent on RhoA or Cdc42 but not on Rac1 ; ( iv ) forced expression of the activating mutants of Rac1, RhoA, or Cdc42 caused a hyperproliferative phenotype of the p19Arf ( -/- ) and p53 ( -/- ) cells and promoted transformation of both cells ; ( v ) RhoA appeared to contribute to p53 regulated cell proliferation by modulating cell cycle machinery, while hyperactivation of RhoA further suppressed a p53 independent apoptotic signal ; and ( vi ) multiple pathways regulated by RhoA, including that of Rho-kinase, were required for RhoA to fully promote the transformation of p53 ( -/- ) cells
D'Amico et al., Cancer Res 2004 (Breast Neoplasms) : p16(INK4a) repressed cyclin D1 expression and transcription ... Repression of cyclin D1 by p16(INK4a) occurred independently of the p16(INK4a)-cdk4 binding function and required a cAMP-response element/activating transcription factor-2 binding site ... p19(ARF) repressed cyclin D1 through a novel distal cis-element at -1137, which bound p53 in chromatin-immunoprecipitation assays
Al-Khalaf et al., PloS one 2011 : p16( INK4a) positively regulates cyclin D1 and E2F1 through negative control of AUF1 ... Furthermore, AUF1 down-regulation increased the expression levels of these genes, while concurrent silencing of AUF1 and p16(INK4a) , using specific siRNAs, restored normal expression of both cyclinD1 and E2F1
Schulze et al., Oncogene 1994 : Activation of the E2F transcription factor by cyclin D1 is blocked by p16INK4 , the product of the putative tumor suppressor gene MTS1
Palmero et al., Oncogene 1997 : In human cells transformed by the large T-antigen of simian virus 40 ( SV40 T-Ag ) and human tumour cell lines that lack a functional retinoblastoma gene product ( pRb ) no cyclin D1-Cdk4 complexes can be detected because all the available Cdk4 is associated with the Cdk-inhibitor p16INK4a
Gill et al., J Clin Invest 1998 : The level of p16(INK4a) , an endogenous inhibitor of the cyclin D1/cdk4 complex decreased