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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