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CDK4 — MYC

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: Complex of CCND2-CDK4-CDKN1B → MYC (increases) Bouchard et al., EMBO J 1999
  Evidence: We nowshow that p27 is rapidly and transiently sequestered by cyclin D2-Cdk4 complexesupon activation of Myc and that cyclin D2 is a direct target gene of Myc.
• KEGG Pathways in cancer: MYC → CDK4 (gene expression, expression)
• KEGG Small cell lung cancer: Complex of MAX-MYC → Complex of CCND1-CDK4-CDK6 (gene expression, expression)
  

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: MYC — CDK4 (direct interaction, enzymatic study) Anders et al., Cancer Cell 2011
• IRef Biogrid Interaction: MYC — CDK4 (direct interaction, two hybrid) Wang et al., Molecular systems biology 2011
• IRef Intact Interaction: MYC — CDK4 (physical association, two hybrid array) Wang et al., Molecular systems biology 2011
• IRef Intact Interaction: MYC — CDK4 (phosphorylation reaction, protein kinase assay) Anders et al., Cancer Cell 2011

Text-mined interactions from Literome

Mateyak et al., Mol Cell Biol 1999 : c-Myc regulates cyclin D-Cdk4 and -Cdk6 activity but affects cell cycle progression at multiple independent points
Hermeking et al., Proc Natl Acad Sci U S A 2000 (Kidney Neoplasms) : c-MYC induced a rapid increase in CDK4 mRNA levels through four highly conserved c-MYC binding sites within the CDK4 promoter
Pawar et al., Oncogene 2004 (Breast Neoplasms) : In order to determine how these opposite functions correlate with the transcriptional activities of the two factors on particular downstream targets, we investigated the roles of USF and c-Myc in expression of CDK4 , a known direct target of c-Myc ... Overexpression of either c-Myc or USF2, but not USF1, stimulated the expression of CDK4 promoter-driven reporter genes in the non-tumorigenic mammary epithelial MCF-10A cells ... Dominant negative mutants specific to either Myc or USF family proteins inhibited reporter gene activity as well as endogenous CDK4 expression, demonstrating involvement of both USF and Myc in CDK4 transcriptional control
Miliani de Marval et al., Mol Cell Biol 2004 (Skin Neoplasms) : Biochemical analysis of the K5-Myc epidermis showed that CDK4 mediates the proliferative activities of Myc by sequestering p21Cip1 and p27Kip1 and thereby indirectly activating CDK2 kinase activity ... These results show that CDK4 mediates the proliferative and oncogenic activities of Myc in vivo through a mechanism that involves the sequestration of specific CDK inhibitors
Amati et al., Frontiers in bioscience : a journal and virtual library 1998 : Cyclin D/CDK4 and CDK6 may conceivably also be activated by Myc , but the circumstances in which this occurs remain to be explored
Alexandrow et al., J Cell Biochem 1998 : Altogether, the data suggest that the presence of excessive Myc protein in keratinocytes can stimulate otherwise noncycling cells to enter the cell cycle, and that this effect of Myc involves both positive effects on E2F-1 associated Cdk-2 and negative effects on Cdk-4 in late G1