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CDKN2A — E2F8

Text-mined interactions from Literome

Hyde et al., Invest Ophthalmol Vis Sci 2002 : Although in the normal lens there do not appear to be unique roles for E2F1 that can not be fulfilled by other E2F family members, in the absence of functional pRB proteins, E2F1 is specifically responsible for the increased expression of E2F3a and p19ARF
Yamasaki et al., Cancer Treat Res 2003 (Neoplasms) : Similarly, E2F1 dependent induction of p19ARF antagonizes the ability of mdm2 to degrade p53, leading to p53 stabilization and potentially p53 mediated apoptosis or cell cycle arrest
Ausserlechner et al., Leukemia 2005 (Precursor Cell Lymphoblastic Leukemia-Lymphoma) : p16(INK4A) expression caused pRB hypophosphorylation and repression of certain E2F target genes
del Arroyo et al., Cell cycle (Georgetown, Tex.) 2007 : E2F dependent induction of p14ARF during cell cycle re-entry in human T cells
Danielian et al., Oncogene 2008 : E2f3 mutant mice typically die around birth and E2f3-deficient cells have a proliferation defect that correlates with impaired E2f target gene activation and also induction of p19(Arf) and p53
Zhang et al., J Cell Biochem 2009 : The regulation of p14ARF gene by E2F transcription factor , which differs from that of classical E2F targets, has recently been attributed to a variant E2F-response element
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
Khleif et al., Proc Natl Acad Sci U S A 1996 (Uterine Cervical Neoplasms) : Given the role of RB in controlling E2F transcription factor activity, we investigated the role of E2F in controlling p16INK4a expression
Halaban et al., Oncogene 1998 : We conclude that neutralization of Rb by E2F1E132, but not the disruption of p16INK4A or p21WAF1/CIP1, resulted in the accumulation of free E2F and cell cycle progression