Gene interactions and pathways from curated databases and text-mining

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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