◀ Back to MYC
CDKN2A — MYC
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
CDKN2A
→
MYC
(increases)
Evidence: studies showing that the ARF gene encoded by the tumor-suppressive gene locus, INK4A, is induced after expression of c-MYC or other mitogenic transcription factors, like E2F [33]. The authors suggest that activation of cell cycle deregulating genes is translated into activation of the ARF gene, which encodes a p53-stabilizing protein [34]. Consistent with this model, fibroblasts from ARF-/- mice are largely refractory to c-MYC-induced apoptosis
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NCI Pathway Database C-MYC pathway:
p14ARF (CDKN2A)
→
MYC/Max/p14ARF complex (MYC-MAX-CDKN2A)
(modification, collaborate)
Datta et al., J Biol Chem 2004*, Qi et al., Nature 2004*
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database C-MYC pathway:
p14ARF (CDKN2A)
→
MYC/Max complex (MYC-MAX)
(modification, collaborate)
Datta et al., J Biol Chem 2004*, Qi et al., Nature 2004*
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database C-MYC pathway:
MYC/Max/p14ARF complex (MYC-MAX-CDKN2A)
→
MYC/Max complex (MYC-MAX)
(modification, collaborate)
Datta et al., J Biol Chem 2004*, Qi et al., Nature 2004*
Evidence: mutant phenotype, physical interaction
-
WikiPathways TP53 Network:
MYC
→
CDKN2A
(activation)
-
WikiPathways Apoptosis:
MYC
→
CDKN2A
(activation)
-
WikiPathways DNA Damage Response (only ATM dependent):
MYC
→
CDKN2A
(activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Jacobs et al., Genes Dev 1999
(Cell Transformation, Neoplastic...) :
Furthermore, Bmi-1 collaborates with Myc in enhancing proliferation and transformation of primary embryo fibroblasts ( MEFs ) in an ink4a-ARF dependent manner, by prohibiting
Myc mediated induction of
p19arf and apoptosis
Jacobs et al., Nat Genet 2000
(Adenocarcinoma...) :
TBX2 represses the Cdkn2a ( p19(ARF) ) promoter and attenuates E2F1,
Myc or HRAS mediated
induction of
Cdkn2a ( p19(ARF) )
Qi et al., Nature 2004
(Cell Transformation, Neoplastic) :
p19ARF directly and differentially
controls the functions of
c-Myc independently of p53
Amente et al., Cancer Biol Ther 2006
:
Finally, we show that
p14ARF down
regulates Myc activated transcription and that this activity can not be addressed to an intrinsic p14ARF repressor domain
Bertwistle et al., Blood 2007
(Disease Progression...) :
Prior to frank lymphoma development, unexpectedly low levels of
Emu-Myc induced
p19Arf or GFP were expressed
Robson et al., BMC genomics 2011
:
Conversely, avoidance of apoptosis in suprabasal keratinocytes may result primarily from the activation of key anti-apoptotic signalling pathways, particularly Igf1-Akt, and induction of an angiogenic response, though intrinsic resistance to
induction of
p19(Arf) by
MYC in suprabasal keratinocytes may contribute