MXD4
MAX dimerization protein 4 | |||||||||||
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Identifiers | |||||||||||
Symbols | MXD4 ; MAD4; MST149; MSTP149 | ||||||||||
External IDs | Template:MGI HomoloGene: 4712 | ||||||||||
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RNA expression pattern | |||||||||||
File:PBB GE MXD4 212346 s at tn.png | |||||||||||
File:PBB GE MXD4 210778 s at tn.png | |||||||||||
File:PBB GE MXD4 212347 x at tn.png | |||||||||||
More reference expression data | |||||||||||
Orthologs | |||||||||||
Template:GNF Ortholog box | |||||||||||
Species | Human | Mouse | |||||||||
Entrez | n/a | n/a | |||||||||
Ensembl | n/a | n/a | |||||||||
UniProt | n/a | n/a | |||||||||
RefSeq (mRNA) | n/a | n/a | |||||||||
RefSeq (protein) | n/a | n/a | |||||||||
Location (UCSC) | n/a | n/a | |||||||||
PubMed search | n/a | n/a |
MAX dimerization protein 4, also known as MXD4, is a human gene.[1]
This gene is a member of the MAD gene family . The MAD genes encode basic helix-loop-helix-leucine zipper proteins that heterodimerize with MAX protein, forming a transcriptional repression complex. The MAD proteins compete for MAX binding with MYC, which heterodimerizes with MAX forming a transcriptional activation complex. Studies in rodents suggest that the MAD genes are tumor suppressors and contribute to the regulation of cell growth in differentiating tissues.[1]
References
Further reading
- Rual JF, Venkatesan K, Hao T; et al. (2005). "Towards a proteome-scale map of the human protein-protein interaction network". Nature. 437 (7062): 1173–8. doi:10.1038/nature04209. PMID 16189514.
- Marcotte R, Chen JM, Huard S, Wang E (2006). "c-Myc creates an activation loop by transcriptionally repressing its own functional inhibitor, hMad4, in young fibroblasts, a loop lost in replicatively senescent fibroblasts". J. Cell. Biochem. 96 (5): 1071–85. doi:10.1002/jcb.20503. PMID 16167342.
- Pope SN, Lee IR (2005). "Yeast two-hybrid identification of prostatic proteins interacting with human sex hormone-binding globulin". J. Steroid Biochem. Mol. Biol. 94 (1–3): 203–8. doi:10.1016/j.jsbmb.2005.01.007. PMID 15862967.
- Hillier LW, Graves TA, Fulton RS; et al. (2005). "Generation and annotation of the DNA sequences of human chromosomes 2 and 4". Nature. 434 (7034): 724–31. doi:10.1038/nature03466. PMID 15815621.
- Gerhard DS, Wagner L, Feingold EA; et al. (2004). "The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC)". Genome Res. 14 (10B): 2121–7. doi:10.1101/gr.2596504. PMID 15489334.
- Jiang DJ, Yu HX, Hexige SY; et al. (2004). "Human liver specific transcriptional factor TCP10L binds to MAD4". J. Biochem. Mol. Biol. 37 (4): 402–7. PMID 15469726.
- Ota T, Suzuki Y, Nishikawa T; et al. (2004). "Complete sequencing and characterization of 21,243 full-length human cDNAs". Nat. Genet. 36 (1): 40–5. doi:10.1038/ng1285. PMID 14702039.
- Strausberg RL, Feingold EA, Grouse LH; et al. (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. doi:10.1073/pnas.242603899. PMID 12477932.
- Kime L, Wright SC (2003). "Mad4 is regulated by a transcriptional repressor complex that contains Miz-1 and c-Myc". Biochem. J. 370 (Pt 1): 291–8. doi:10.1042/BJ20021679. PMID 12418961.
- Cairo S, Merla G, Urbinati F; et al. (2001). "WBSCR14, a gene mapping to the Williams--Beuren syndrome deleted region, is a new member of the Mlx transcription factor network". Hum. Mol. Genet. 10 (6): 617–27. PMID 11230181.
- Billin AN, Eilers AL, Queva C, Ayer DE (2000). "Mlx, a novel Max-like BHLHZip protein that interacts with the Max network of transcription factors". J. Biol. Chem. 274 (51): 36344–50. PMID 10593926.
- Hurlin PJ, Quéva C, Koskinen PJ; et al. (1996). "Mad3 and Mad4: novel Max-interacting transcriptional repressors that suppress c-myc dependent transformation and are expressed during neural and epidermal differentiation". EMBO J. 14 (22): 5646–59. PMID 8521822.
External links
- MXD4+protein,+human at the US National Library of Medicine Medical Subject Headings (MeSH)
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This article incorporates text from the United States National Library of Medicine, which is in the public domain.