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Gene Review

MAFA  -  v-maf avian musculoaponeurotic...

Homo sapiens

Synonyms: Pancreatic beta-cell-specific transcriptional activator, RIPE3b1, Transcription factor MafA, Transcription factor RIPE3b1, V-maf musculoaponeurotic fibrosarcoma oncogene homolog A, ...
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Disease relevance of MAFA

  • AIMS/HYPOTHESIS: Effects of the transcription factor v-maf musculoaponeurotic fibrosarcoma oncogene homologue A (MAFA) on the regulation of beta cell gene expression and function were investigated [1].

High impact information on MAFA

  • Here we report that a prototype inhibitory receptor, the mast cell function-associated antigen (MAFA), selectively regulates the FcvarepsilonRI stimulus-response coupling network and the subsequent de novo production and secretion of inflammatory mediators [2].
  • Here, we report cloning of the human mafA (hMafA) and demonstrate that it can specifically bind the insulin enhancer element RIPE3b and activate insulin-gene expression [3].
  • The cytoplasmic tail of MAFA contains a YXXL (YSTL) motif, which is conserved among related C-type lectins and is an essential element in the immunoreceptor tyrosine-based activation motifs [4].
  • Here we report that the MAFA is expressed as both a monomer and a homodimer [4].
  • However, we found that mutations in either the ICE or the RIPE3b1 element reduced glucose-responsive expression from transfected 5'-flanking rat insulin II gene constructs [5].

Biological context of MAFA


Anatomical context of MAFA

  • This glycoprotein, named mast cell function-associated antigen (MAFA), was also shown to interfere with the coupling cascade of the type 1 Fc epsilon receptor upstream to phospholipase C gamma 1 activation by protein-tyrosine kinases [4].
  • Islet cell differentiation in liver by combinatorial expression of transcription factors Neurogenin-3, BETA2, and RIPE3b1 [8].
  • Taken together, these results of distinct methodologies suggest that MAFA functions within raft microdomains of the RBL-2H3 cell membrane and thus in close proximity to the FcepsilonRI which themselves signal from within the raft environment [9].
  • Compartmentalization of the Type I Fcepsilon receptor and MAFA on mast cell membranes [9].

Associations of MAFA with chemical compounds

  • Glucose influenced DNA-binding activity of MAFA in rat islets in a bell-shaped manner [1].
  • We used cholera toxin B subunit (CTB) to cluster the raft component ganglioside GM1 and studied the effects of this perturbation on rotation of FcepsilonRI and MAFA by time-resolved phosphorescence anisotropy of erythrosin-conjugated probes [9].
  • Evaluation of raft localization of FcepsilonRI and MAFA using sucrose gradient ultracentrifugation of Triton X-100 treated membrane fragments demonstrates that a significant fraction of MAFA molecules sediments with rafts when FcepsilonRI is clustered by antigen or when MAFA itself is clustered by mAb G63 [9].
  • Collectively, the data suggested that removal of a tyrosine(s) within RIPE3b1 prevented activator binding to insulin C1 control element sequences [7].
  • The loss in RIPE3b1 binding activity was prevented by inhibitors of tyrosine phosphatases (sodium orthovanadate and sodium molybdate) but not by inhibitors of serine/threonine phosphatases (sodium fluoride, okadaic acid, and microcystin LR) [7].

Other interactions of MAFA

  • In fragment D, cotransfection of oligonucleotide that confers RIPE3b1 activator decreased the glucose-stimulated promoter activity, but the other oligonucleotide that confers STF-1 did not [6].

Analytical, diagnostic and therapeutic context of MAFA


  1. MAFA controls genes implicated in insulin biosynthesis and secretion. Wang, H., Brun, T., Kataoka, K., Sharma, A.J., Wollheim, C.B. Diabetologia (2007) [Pubmed]
  2. Selective inhibition of the FcvarepsilonRI-induced de novo synthesis of mediators by an inhibitory receptor. Abramson, J., Licht, A., Pecht, I. EMBO J. (2006) [Pubmed]
  3. Identification of beta-cell-specific insulin gene transcription factor RIPE3b1 as mammalian MafA. Olbrot, M., Rud, J., Moss, L.G., Sharma, A. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  4. A secretion inhibitory signal transduction molecule on mast cells is another C-type lectin. Guthmann, M.D., Tal, M., Pecht, I. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  5. Glucose-induced transcription of the insulin gene is mediated by factors required for beta-cell-type-specific expression. Sharma, A., Stein, R. Mol. Cell. Biol. (1994) [Pubmed]
  6. Identification and characterization of a glucose-responsiveness region upstream of human insulin gene in transfected HIT-T 15 cells. Ohtani, K., Shimizu, H., Kato, Y., Mori, M. Biochem. Biophys. Res. Commun. (1998) [Pubmed]
  7. The DNA binding activity of the RIPE3b1 transcription factor of insulin appears to be influenced by tyrosine phosphorylation. Matsuoka , T., Zhao, L., Stein, R. J. Biol. Chem. (2001) [Pubmed]
  8. Islet cell differentiation in liver by combinatorial expression of transcription factors Neurogenin-3, BETA2, and RIPE3b1. Song, Y.D., Lee, E.J., Yashar, P., Pfaff, L.E., Kim, S.Y., Jameson, J.L. Biochem. Biophys. Res. Commun. (2007) [Pubmed]
  9. Compartmentalization of the Type I Fcepsilon receptor and MAFA on mast cell membranes. Barisas, B.G., Smith, S.M., Liu, J., Song, J., Hagen, G.M., Pecht, I., Roess, D.A. Biophys. Chem. (2007) [Pubmed]
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