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BAX — E2F1
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
O'Hare et al., J Biol Chem 2000
:
We show that adenovirus mediated expression of
E2F-1 in CGNs results in apoptotic death, which is independent of p53,
dependent upon
Bax , and associated with caspase 3-like activity
Atienza et al., Int J Mol Med 2000
(Stomach Neoplasms) :
Bax levels also increased in
response to
E2F-1 gene transfer, alone and in combination with roscovitine
Suzuki et al., Int J Cancer 2000
(Mouth Neoplasms...) :
TSA
enhanced the protein expression of p21 ( WAF1 ), CREB binding protein, cyclinE, cyclin A, Bak and
Bax , while it reduced the expression of
E2F-1 , E2F-4, HDAC1, p53 and hyperphosphorylated form of Rb
Chen et al., Invest Ophthalmol Vis Sci 2000
:
Expression of either
E2F1 or E2F2 was
sufficient to induce the transcription of cyclins ( A2, B1, and E ), as well as p53 and
Bax in the lens fibercells
Shu et al., Neuro Oncol 2000
(Glioma) :
BAX induction did not
follow E2F1 overexpression or irradiation in the glioma cell lines tested
Sola et al., J Biol Chem 2003
:
Moreover, in the absence of TGF-beta1, UDCA prevented
induction of p53 and
Bax by overexpression of
E2F-1 and p53, respectively ( p < 0.05 )
Ramalho et al., J Neurochem 2004
:
Notably, TUDCA modulated Abeta induced apoptosis,
E2F-1 induction , p53 stabilization and
Bax expression ... Notably, TUDCA modulated Abeta induced apoptosis,
E2F-1 induction , p53 stabilization and
Bax expression
Hao et al., BMC cancer 2007
(Melanoma) :
E2F-1 induced
Bax translocation was shown by immunocytochemistry
Espada et al., PloS one 2012
(Adrenal Gland Neoplasms...) :
ROS accumulation followed
E2F1 induction and treatment with the antioxidant N-acetylcysteine,
inhibited E2F1 induced
Bax translocation to mitochondria and subsequent apoptosis