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CDKN2A — ID1

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: CDKN2A → ID1 (decreases) Ouyang et al., Carcinogenesis 2002*
  Evidence: p16INK4a was much lower or undetectable in all the Id-1 expressing clones of LNCaP cells, while approximately 2 to 3 fold increases in p16INK4a levels was observed in the controls and in the Id-1 negative clones, suggesting that expression of Id-1 reduced the p16INK4a protein levels in LNCaP cells.

Text-mined interactions from Literome

Alani et al., Proc Natl Acad Sci U S A 2001 : We also show that Id1 is able to directly inhibit p16/Ink4a but not p19/ARF promoter activity via its HLH domain, and that Id1 inhibits transcriptional activation at E-boxes within the p16/Ink4a promoter
Polsky et al., Cancer Res 2001 (Melanoma) : Because the p16/Ink4a protein has been demonstrated to be inactivated in subsets of familial and sporadic melanomas, we sought to determine whether Id1 regulation of p16/Ink4a expression might be involved in the development of this human tumor ... These data suggest a role for Id1 in regulating p16/Ink4a expression in early melanomas and demonstrate that later genetic changes may provide for irreversible loss of p16 expression in advanced stages of this tumor
Lee et al., Carcinogenesis 2003 (Carcinoma, Hepatocellular...) : As p16INK4a protein is inactivated in hepatocellular carcinoma ( HCC ), we aimed to investigate the role of Id-1 in regulating p16INK4a expression during the development of HCC in HCC patients and direct ectopic Id-1 introduction into the PLC/PRF/5 HCC cell line
Zheng et al., J Biol Chem 2004 : Silencing Id1 expression in young cells by RNA interference induced an increased p16(INK4a) level and premature cellular senescence, whereas silencing E47 expression inhibited the expression of p16(INK4a) and delayed the onset of senescent phenotype
Hui et al., Int J Cancer 2006 (Carcinoma, Squamous Cell...) : However, overexpression of Id-1 had no effect on the pRB, CDK4 and p16INK4A expressions