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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
• 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 *

• IRef Bind Interaction: MYC — CDKN2A Qi et al., Nature 2004*
• IRef Bind_translation Interaction: MYC — CDKN2A (coimmunoprecipitation) Qi et al., Nature 2004*
• IRef Biogrid Interaction: MYC — CDKN2A (physical association, affinity chromatography technology) Herkert et al., J Cell Biol 2010*
• IRef Biogrid Interaction: MYC — CDKN2A (physical association, affinity chromatography technology) Amente et al., FEBS Lett 2007*
• IRef Biogrid Interaction: MYC — CDKN2A (physical association, affinity chromatography technology) Zhang et al., Proc Natl Acad Sci U S A 2013*
• IRef Hprd Interaction: MYC — CDKN2A (in vivo) Qi et al., Nature 2004*

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