Pathways - manually collected, often from reviews:
OpenBEL Selventa BEL large corpus:
MYC
→
Complex of HIF1A-MAX
(decreases, HIF1A/MAX Activity)
Evidence: A recent study suggests another mechanism by which HIF1? inhibits MYC function through binding MAX and thereby displacing MYC4,48.
OpenBEL Selventa BEL large corpus:
CDKN1A
→
Complex of HIF1A-MYC
(increases)
Evidence: a study using HCT116 colon carcinoma cells depleted of either p53 or p21 found that HIF1? is required for cellcycle arrest through the induction of p21 by a direct interaction between HIF1? and MYC39.
OpenBEL Selventa BEL large corpus:
MYC
→
HIF1A
(decreases, HIF1A Activity)
Evidence: The mechanism by which HIF mediates these effects appears to be through inhibition of C-Myc activity. The mechanism by which HIF mediates these effects appears to be through inhibition of C-Myc activity. HIF-1 was found to negatively regulate C-Myc activity and mitochondrial respiration through transcriptional activation of the C-Myc repressor, MXI-1, and through regulation of C-Myc protein stability.
OpenBEL Selventa BEL large corpus:
MYC
→
HIF1A
(decreases, HIF1A Activity, MYC Activity)
Evidence: in VHL-deficient renal cell carcinoma cells, HIF-1 can induce a decrease in respiration and mitochondrial biogenesis by negatively regulating c-myc activity and, thereby reducing the expression of the transcriptional coactivator protein PGC-1b, resulting in reduced cellular respiration [39].
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *