◀ Back to MYC
BAX — MYC
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
BAX
→
MYC
(increases)
Evidence: Overexpression of c- MYC upregulates endogenous pro-apoptotic Bax mRNA and protein expression in human cells.
-
WikiPathways Apoptosis:
MYC
→
BAX
(activation)
Text-mined interactions from Literome
Ceballos et al., Oncogene 2000
(Blast Crisis) :
Also, p53 mediated up-regulation of p21WAF1 mRNA protein were significantly
reduced by
c-Myc , while
Bax levels were unaffected
Shiotani et al., Carcinogenesis 2001
:
After treatment with Trp-P-1,
c-Myc protein level increased in a time dependent manner and p53 protein also
increased transiently with a subsequent increase in
Bax protein level
Soucie et al., Mol Cell Biol 2001
:
During apoptosis,
Bax translocation to the mitochondria occurs in the
presence or absence of
Myc expression ... These results demonstrate a
role for
Myc in the regulation of
Bax activation during apoptosis
Dansen et al., J Biol Chem 2006
(Neoplasm Invasiveness...) :
Using a switchable mouse model of Myc induced apoptosis in pancreatic beta cells, we have shown that
Myc induces apoptosis in vivo exclusively through
Bax but not Bak
Albihn et al., J Cell Biochem 2006
:
Apoptosis was paralleled by
c-Myc dependent
Bax-activation after etoposide and doxorubicin treatment, but not after cisplatin administration
Cao et al., J Biol Chem 2008
:
c-Myc and caspase-2 are
involved in activating
Bax during cytotoxic drug induced apoptosis ... Although knockdown of c-Myc or caspase-2 does not affect Bax expression, caspase-2 is important for cytosolic
Bax to integrate into the outer mitochondrial membrane, and
c-Myc is
critical for oligomerization of Bax once integrated into the membrane