Property Summary

NCBI Gene PubMed Count 103
Grant Count 24
R01 Count 18
Funding $2,839,322.75
PubMed Score 104.82
PubTator Score 789.79

Knowledge Summary


No data available


  Differential Expression (12)

Disease log2 FC p
esophageal adenocarcinoma -1.100 0.018
psoriasis -2.000 0.000
osteosarcoma -1.713 0.000
astrocytoma 1.200 0.011
Crohn's disease -1.025 0.000
ulcerative colitis -1.108 0.008
juvenile dermatomyositis 1.401 0.000
acute quadriplegic myopathy 1.041 0.000
non primary Sjogren syndrome sicca 1.200 0.011
subependymal giant cell astrocytoma -1.894 0.007
ovarian cancer -1.900 0.000
dermatomyositis 1.300 0.002

Gene RIF (32)

26670126 our results confirm that MAX is a tumor suppressor gene for renal oncocytomas
26555092 In addition, loss of function mutation of the MAX gene was identified for the first time in GIST, and a broader role for MAX in GIST progression was suggested. mechanism for a subset of sporadic gastrointestinal stromal tumors
26474287 Celastrol and some of its quinone methidecontaining analogs directly inhibit c-Myc-Max heterodimers in tumor cells.
26070438 The introduction of wild-type MAX cDNA into PC12 cells significantly decreased MYC's ability to bind to canonical E-boxes, while pathogenic MAX proteins were not able to fully repress MYC activity. Further clinical and molecular evaluation of variant carriers corroborated the results obtained with the functional assessment.
25875098 We confirmed that these dimeric inhibitors directly bind to Myc blocking its interaction with Max and affect transcription of MYC dependent genes.
25451222 Hypoxia reduces MAX expression in endothelial cells by unproductive splicing
24857747 MYC is part of a network of bHLHLZ proteins centered on the MYC heterodimeric partner MAX and its counterpart, the MAX-like protein MLX.
24731854 Here we review the activities of MYC, MNT and other MAX interacting proteins in the setting of T and B cell activation and oncogenesis
24676840 Max mutation is associated with pheochromocytomas and paragangliomas.
24657798 Myc and its obligate heterodimeric partner, Max, are integral to the coordinated recruitment and post-translational modification of components of the core transcriptional machinery.

AA Sequence

SSESEPEEPQSRKKLRMEAS                                                      141 - 160

Text Mined References (110)

PMID Year Title
26670126 2016 Complex MAX Rearrangement in a Family With Malignant Pheochromocytoma, Renal Oncocytoma, and Erythrocytosis.
26555092 2015 Somatic loss of function mutations in neurofibromin 1 and MYC associated factor X genes identified by exome-wide sequencing in a wild-type GIST case.
26474287 2015 Direct inhibition of c-Myc-Max heterodimers by celastrol and celastrol-inspired triterpenoids.
26267534 2015 Small Molecule Inhibition of ERK Dimerization Prevents Tumorigenesis by RAS-ERK Pathway Oncogenes.
26070438 2015 Functional and in silico assessment of MAX variants of unknown significance.
25875098 2015 Reversible linkage of two distinct small molecule inhibitors of Myc generates a dimeric inhibitor with improved potency that is active in myc over-expressing cancer cell lines.
25609649 2015 Proteomic analyses reveal distinct chromatin-associated and soluble transcription factor complexes.
25451222 2014 Hypoxia reduces MAX expression in endothelial cells by unproductive splicing.
25416956 2014 A proteome-scale map of the human interactome network.
25175806 2014 Drugging MYCN through an allosteric transition in Aurora kinase A.