Recombinant Human Protein max (MAX)

1. MAX inactivation is a common event in GIST progression, fostering cell cycle activity in early GISTs. PMID:28270683
2. MAX to MYCN ratio that can account for tumour progression and clinical outcome in neuroblastoma. PMID:29408445
3. To our knowledge, this is the first report of an association between dysregulation of the MAX-MYC network in the brain and a behavior, suggesting a novel approach for exploiting the neuroplasticity associated with depression PMID:27727240
4. Sequence-specific DNA binding by MYC/MAX to low-affinity non-E-box motifs PMID:28719624
5. The SDHA, TMEM127, MAX, and SDHAF2 genes contribute to hereditary pheochromocytoma and paraganglioma. PMID:28384794
6. These results suggest that the wild type Max homodimer is important for attenuating the binding of c-Myc to specific and non-specific DNA, whereas alternative splicing (e.g. DeltaMax) is unable to do so. Conversely, the splicing of Max into DeltaMax could provoke an increase in overall chromatin bound c-Myc. PMID:28350847
7. evidence that MAX can 'sense' the oxidation status of 5mCpGs, and that cancer-associated mutations in MAX differentially affect binding to these features PMID:27903915
8. The mechanism of inhibition of c-Myc transcriptional activity by Miz-1 that binds c-Myc while competing for binding with Max has been described. PMID:27859590
9. 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. PMID:26070438
10. Celastrol and some of its quinone methidecontaining analogs directly inhibit c-Myc-Max heterodimers in tumor cells. PMID:26474287
11. our results confirm that MAX is a tumor suppressor gene for renal oncocytomas PMID:26670126
12. 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 PMID:26555092
13. We confirmed that these dimeric inhibitors directly bind to Myc blocking its interaction with Max and affect transcription of MYC dependent genes. PMID:25875098
14. MYC is part of a network of bHLHLZ proteins centered on the MYC heterodimeric partner MAX and its counterpart, the MAX-like protein MLX. PMID:24857747
15. Myc and its obligate heterodimeric partner, Max, are integral to the coordinated recruitment and post-translational modification of components of the core transcriptional machinery. PMID:24657798
16. Here we review the activities of MYC, MNT and other MAX interacting proteins in the setting of T and B cell activation and oncogenesis PMID:24731854
17. MAX mutations remain unusual events in Swedish patients with pheochromocytoma and paraganglioma tumours. PMID:23743562
18. Hypoxia reduces MAX expression in endothelial cells by unproductive splicing PMID:25451222
19. Genetic and molecular findings provide powerful evidence that MAX is a tumor-suppressor gene involved in SCLC development. PMID:24362264
20. Max mutation is associated with pheochromocytomas and paragangliomas. PMID:24676840
21. Delta Max, but not full-length Max, rescues Myc-dependent glycolytic gene expression upon induced EGFRvIII loss, and correlates with hnRNPA1 expression and downstream Myc-dependent gene transcription in patients. PMID:23707073
22. Data show that Sirt1, p53, and p38(MAPK) are involved in the detrimental phenotype of Max-null ESCs. Analyses revealed these proteins are involved at varying levels to one another in the hierarchy of the pathway leading to cell death in Max-null ESCs. PMID:22696478
23. germline mutations in MAX are responsible for 1.12% of hereditary and sporadic pheochromocytoma and paraganglioma in patients without evidence of other known mutations PMID:22452945
24. New structural determinants for c-Myc specific heterodimerization with Max and development of a novel homodimeric c-Myc b-HLH-LZ. PMID:22733550
25. Max b-HLH-LZ can transduce into cells and inhibit c-Myc transcriptional activities PMID:22384171
26. Genetic variants in MAX does not contribute to the development of Lynch syndrome. PMID:22086303
27. The E-box binding factors Max/Mnt, MITF, and USF1 act coordinately with FoxO to regulate expression of proapoptotic and cell cycle control genes by phosphatidylinositol 3-kinase/Akt/glycogen synthase kinase 3 signaling. PMID:21873430
28. The transcription factors Max and RXRalpha bind directly to the miR-193a promoter and inhibit miR-193a expression during transformation, thereby activating the PLAU and K-Ras oncogenes. PMID:21670079
29. MAX mutations are associated with hereditary pheochromocytoma. PMID:21685915
30. Enforced miR-22 expression presumably lowers Max levels available for Myc binding, which differentially influenced the transcription of downstream targets of the Myc-Max complex. PMID:20214878
31. downregulation of MYCN was reflected in a decreased MYCN/Max DNA-binding activity while the Mnt/Max binding did not change during differentiation PMID:15258910
32. High levels of Max and stress-induced NFkappaB activation may result in elevated expression of Fas ligand in human lung cancer cells and possibly contribute to Fas ligand-associated immune escape mechanisms. PMID:15302589
33. C6-cer inhibited the DNA-binding function of the c-Myc/Max oncogene PMID:16201965
34. Binding affinities & thermodynamics of dimerization of Max-Max homodimer & c-Myc-Max & Mad-Max heterodimers were determined.c-Myc & Max form most stable heterodimer.Polylysine had little effect, polyglutamic acid stabilized both heterodimers & homodimers. PMID:16475822
35. results uncover novel post-translational modifications of Max and suggest the potential regulation of specific Max complexes by p300 and reversible acetylation PMID:17217336
36. The switch from Mnt-Max to Myc-Max during bile duct ligation (cholestasis) and in hepatocytes treated with lithocholic acid is responsible for the induction in p53 and cyclin D1 expression and contributes to apoptosis. PMID:19086036

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HGNC: 6913

UNIGENE: Hs.285354

KEGG: hsa:4149

STRING: 9606.ENSP00000351490

OMIM: 154950