Mothers against decapentaplegic homolog 6

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SMAD family member 6
Identifiers
Symbols SMAD6 ; AOVD2; HsT17432; MADH6; MADH7
External IDs OMIM602931 MGI1336883 HomoloGene4079 GeneCards: SMAD6 Gene
RNA expression pattern
PBB GE SMAD6 207069 s at tn.png
PBB GE SMAD6 209886 s at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 4091 17130
Ensembl ENSG00000137834 ENSMUSG00000036867
UniProt O43541 O35182
RefSeq (mRNA) NM_001142861 NM_008542
RefSeq (protein) NP_001136333 NP_032568
Location (UCSC) Chr 15:
66.99 – 67.07 Mb
Chr 9:
63.95 – 64.02 Mb
PubMed search [1] [2]

SMAD family member 6, also known as SMAD6, is a protein that in humans is encoded by the SMAD6 gene.[1]

SMAD6 is a protein that, as its name describes, is a homolog of the Drosophila gene "mothers against decapentaplegic". It belongs to the SMAD family of proteins, which belong to the TGFβ superfamily of modulators. Like many other TGFβ family members SMAD6 is involved in cell signalling. It acts as a regulator of TGFβ family (such as bone morphogenetic proteins) activity by competing with SMAD4 and preventing the transcription of SMAD4's gene products. There are two known isoforms of this protein.

Nomenclature[edit]

The SMAD proteins are homologs of both the drosophila protein, mothers against decapentaplegic (MAD) and the C. elegans protein SMA. The name is a combination of the two. During Drosophila research, it was found that a mutation in the gene MAD in the mother repressed the gene decapentaplegic in the embryo. The phrase "Mothers against" was added since mothers often form organizations opposing various issues, e.g., Mothers Against Drunk Driving, or MADD.

Interactions[edit]

Mothers against decapentaplegic homolog 6 has been shown to interact with HOXC8,[2] Mothers against decapentaplegic homolog 7,[3] PIAS4,[4] STRAP[5] and MAP3K7.[6][7]

References[edit]

  1. ^ "Entrez Gene: SMAD6 SMAD family member 6". 
  2. ^ Bai, S; Shi X, Yang X, Cao X (March 2000). "Smad6 as a transcriptional corepressor". J. Biol. Chem. (UNITED STATES) 275 (12): 8267–70. doi:10.1074/jbc.275.12.8267. ISSN 0021-9258. PMID 10722652. 
  3. ^ Topper, J N; Cai J, Qiu Y, Anderson K R, Xu Y Y, Deeds J D, Feeley R, Gimeno C J, Woolf E A, Tayber O, Mays G G, Sampson B A, Schoen F J, Gimbrone M A, Falb D (August 1997). "Vascular MADs: Two novel MAD-related genes selectively inducible by flow in human vascular endothelium". Proc. Natl. Acad. Sci. U.S.A. (UNITED STATES) 94 (17): 9314–9. doi:10.1073/pnas.94.17.9314. ISSN 0027-8424. PMC 23174. PMID 9256479. 
  4. ^ Imoto, Seiyu; Sugiyama Kenji, Muromoto Ryuta, Sato Noriko, Yamamoto Tetsuya, Matsuda Tadashi (September 2003). "Regulation of transforming growth factor-beta signaling by protein inhibitor of activated STAT, PIASy through Smad3". J. Biol. Chem. (United States) 278 (36): 34253–8. doi:10.1074/jbc.M304961200. ISSN 0021-9258. PMID 12815042. 
  5. ^ Datta, P K; Moses H L (May 2000). "STRAP and Smad7 Synergize in the Inhibition of Transforming Growth Factor β Signaling". Mol. Cell. Biol. (UNITED STATES) 20 (9): 3157–67. doi:10.1128/MCB.20.9.3157-3167.2000. ISSN 0270-7306. PMC 85610. PMID 10757800. 
  6. ^ Kimura, N; Matsuo R, Shibuya H, Nakashima K, Taga T (June 2000). "BMP2-induced apoptosis is mediated by activation of the TAK1-p38 kinase pathway that is negatively regulated by Smad6". J. Biol. Chem. (UNITED STATES) 275 (23): 17647–52. doi:10.1074/jbc.M908622199. ISSN 0021-9258. PMID 10748100. 
  7. ^ Yanagisawa, M; Nakashima K, Takeda K, Ochiai W, Takizawa T, Ueno M, Takizawa M, Shibuya H, Taga T (December 2001). "Inhibition of BMP2-induced, TAK1 kinase-mediated neurite outgrowth by Smad6 and Smad7". Genes Cells (England) 6 (12): 1091–9. doi:10.1046/j.1365-2443.2001.00483.x. ISSN 1356-9597. PMID 11737269. 

Further reading[edit]