Gene interactions and pathways from curated databases and text-mining

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MAX — MYC

Pathways - manually collected, often from reviews:

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

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Kirch et al., Oncogene 1999 : Expression of human p53 requires synergistic activation of transcription from the p53 promoter by AP-1, NF-kappaB and Myc/Max
Harris et al., J Biol Chem 2002 (Neuroblastoma) : Using transient transfection assays, we show that the Pax-3 promoter is activated by both N-Myc-Max and c-Myc-Max
Chung et al., Cancer Lett 2002 (Stomach Neoplasms) : Unsaturated fatty acids bind Myc-Max transcription factor and inhibit Myc-Max-DNA complex formation
Wiener et al., Exp Cell Res 2004 (Carcinoma, Non-Small-Cell Lung...) : Our results revealed that inhibition of c-Myc/Max did not substantially reduce basal levels of Fas ligand promoter activity, nor did overexpression of c-Myc significantly induce promoter activity ... Our results revealed that inhibition of c-Myc/Max did not substantially reduce basal levels of Fas ligand promoter activity, nor did overexpression of c-Myc significantly induce promoter activity
Wang et al., J Cell Physiol 2006 (Carcinoma, Hepatocellular...) : Since the participation of c-Myc protein in transcription requires its dimerization with Max protein, we examined the Myc-Max association in Cpd 5-treated cells and found that Cpd 5 suppressed Myc-Max dimerization
Zhao et al., Am J Hum Genet 2007 (Genetic Predisposition to Disease) : Third, we found that an allele of SNP4 ( rs4950928 ), the tagging SNP of CCC, impaired the MYC/MAX regulated transcriptional activation of CHI3L1 by altering the transcriptional-factor consensus sequences, and this may be responsible for the decreased expression of the CCC haplotype
Berberich et al., Genes Dev 1992 : Casein kinase II inhibits the DNA binding activity of Max homodimers but not Myc/Max heterodimers ... In contrast, phosphorylation of Max and/or Myc by CKII had no inhibitory or stimulatory effect on the DNA binding activity of Myc/Max heterodimers
Boult et al., Br J Cancer 2008 (Adenocarcinoma...) : Overexpression of c-MYC and MAD proteins in SEG1 cells resulted in differential expression of MYC/MAX/MAD network members and reciprocal changes in proliferation ... Overexpression of c-MYC and MAD proteins in SEG1 cells resulted in differential expression of MYC/MAX/MAD network members and reciprocal changes in proliferation
Yang et al., Hepatology 2009 (Cholestasis...) : Switch from Mnt-Max to Myc-Max induces p53 and cyclin D1 expression and apoptosis during cholestasis in mouse and human hepatocytes ... Switch from Mnt-Max to Myc-Max induces p53 and cyclin D1 expression and apoptosis during cholestasis in mouse and human hepatocytes ... Mnt-Max also binds the E-box sequence but serves as a repressor and inhibits the enhancer activity of Myc-Max ... The current work tested the hypothesis that the switch from Mnt-Max to Myc-Max is responsible for p53 and cyclin D1 up-regulation and apoptosis during cholestasis ... The current work tested the hypothesis that the switch from Mnt-Max to Myc-Max is responsible for p53 and cyclin D1 up-regulation and apoptosis during cholestasis
Chappell et al., Genes Dev 2013 : In this study, we define a mechanism for this by showing that MYC/MAX complexes suppress ERK activity by transcriptionally regulating two members of the dual-specificity phosphatase ( DUSP ) family
Gaubatz et al., EMBO J 1995 : The second mechanism involves a specific interaction between C-terminal domains of AP-2 and the BR/HLH/LZ domain of Myc, but not Max or Mad. Binding of AP-2 to Myc does not preclude association of Myc with Max, but impairs DNA binding of the Myc/Max complex and inhibits transactivation by Myc even in the absence of an overlapping AP-2 binding site
Boyd et al., Mol Cell Biol 1997 : To determine whether binding of Myc-Max or USF is critical for cad growth regulation, we analyzed promoter constructs which contain mutations in the nucleotides flanking the E box ... This result supports the conclusion that binding of Myc-Max , but not USF, is essential for cad regulation
Schneider et al., Curr Top Microbiol Immunol 1997 (Cell Transformation, Neoplastic) : Myc transformed cells are also characterised by the loss of expression of a number of genes and this repressive effect of Myc on gene expression may not be mediated by the Myc/Max complex
Facchini et al., FASEB J 1998 (Cell Transformation, Neoplastic) : Finally, we explore whether direct transactivation of cellular genes by Myc-Max heterodimers is sufficient for the growth promoting and transforming activities of Myc or whether other molecular activities of Myc, such as Myc mediated repression, may play a key role
Zaffran et al., Development 1998 : pit encodes a DEAD-box RNA helicase, a family of proteins involved in the control of RNA structure in many cellular processes and its closest homologue is a human DEAD-box RNA helicase, MrDb , whose corresponding gene transcription is directly activated by Myc-Max heterodimers ( Grandori, C., Mac, J., Siëbelt, F., Ayer, D. E. and Eisenman, R. N. ( 1996 ) EMBO J. 15, 4344-4357 )
Qin et al., Blood 1999 (Lymphoma, T-Cell, Cutaneous...) : Interleukin-7 (IL-7) and IL-15 , which have been identified as growth factors for CTCL cells, stimulated the DNA binding of JunD and two novel c-Myc recognition site ( E-box ) binding proteins, but not the DNA binding of c-Myc/Max heterodimers ... Interleukin-7 (IL-7) and IL-15, which have been identified as growth factors for CTCL cells, stimulated the DNA binding of JunD and two novel c-Myc recognition site ( E-box ) binding proteins, but not the DNA binding of c-Myc/Max heterodimers