Difference between revisions of "Part:BBa K3450005"
 
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MafA: A transcription factor that drives insulin expression in response to glucose.
 
  
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<partinfo>BBa_K3450005 short</partinfo>
  
 
V-maf musculoaponeurotic fibrosarcoma oncogene homolog A (MAFA) belongs to the MAF family of basic leucine zipper transcription factors. MAFA binds to a conserved insulin enhancer element called RIPE3b/C1-A2 and activates insulin gene expression.[1] It is exclusively expressed in the beta islet cells in humans. The subcellular dispersal of MAFA is glucose independent but its DNA binding activity is dependent on the glucose concentration.[3]
 
V-maf musculoaponeurotic fibrosarcoma oncogene homolog A (MAFA) belongs to the MAF family of basic leucine zipper transcription factors. MAFA binds to a conserved insulin enhancer element called RIPE3b/C1-A2 and activates insulin gene expression.[1] It is exclusively expressed in the beta islet cells in humans. The subcellular dispersal of MAFA is glucose independent but its DNA binding activity is dependent on the glucose concentration.[3]
 
Transient expression of PDX1, NEUROG3, and/or MAFA has been successfully used to reprogram intestinal crypt cells into glucose-responsive insulin-producing neoislet cells.[2]
 
Transient expression of PDX1, NEUROG3, and/or MAFA has been successfully used to reprogram intestinal crypt cells into glucose-responsive insulin-producing neoislet cells.[2]
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===Usage and Biology===
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<span class='h3bb'>Sequence and Features</span>
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<partinfo>BBa_K3450005 SequenceAndFeatures</partinfo>
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===Functional Parameters===
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<partinfo>BBa_K3450005 parameters</partinfo>
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References
 
References
  
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[1 ]Zhu, Y., Liu, Q., Zhou, Z. & Ikeda, Y. PDX1 , Neurogenin-3 , and MAFA : critical transcription regulators for beta cell development and regeneration. 1–7 (2017). doi:10.1186/s13287-017-0694-z  
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[1] Zhu, Y., Liu, Q., Zhou, Z. & Ikeda, Y. PDX1 , Neurogenin-3 , and MAFA : critical transcription regulators for beta cell development and regeneration. 1–7 (2017). doi:10.1186/s13287-017-0694-z  
 
https://stemcellres.biomedcentral.com/track/pdf/10.1186/s13287-017-0694-z  
 
https://stemcellres.biomedcentral.com/track/pdf/10.1186/s13287-017-0694-z  
  

Latest revision as of 15:18, 26 October 2020


MafA: A transcription factor that drives insulin expression in response to glucose.

V-maf musculoaponeurotic fibrosarcoma oncogene homolog A (MAFA) belongs to the MAF family of basic leucine zipper transcription factors. MAFA binds to a conserved insulin enhancer element called RIPE3b/C1-A2 and activates insulin gene expression.[1] It is exclusively expressed in the beta islet cells in humans. The subcellular dispersal of MAFA is glucose independent but its DNA binding activity is dependent on the glucose concentration.[3] Transient expression of PDX1, NEUROG3, and/or MAFA has been successfully used to reprogram intestinal crypt cells into glucose-responsive insulin-producing neoislet cells.[2]

Sequence and Features


Assembly Compatibility:
  • 10
    COMPATIBLE WITH RFC[10]
  • 12
    INCOMPATIBLE WITH RFC[12]
    Illegal NheI site found at 12
  • 21
    INCOMPATIBLE WITH RFC[21]
    Illegal BglII site found at 921
  • 23
    COMPATIBLE WITH RFC[23]
  • 25
    INCOMPATIBLE WITH RFC[25]
    Illegal AgeI site found at 223
  • 1000
    COMPATIBLE WITH RFC[1000]



References

[1] Zhu, Y., Liu, Q., Zhou, Z. & Ikeda, Y. PDX1 , Neurogenin-3 , and MAFA : critical transcription regulators for beta cell development and regeneration. 1–7 (2017). doi:10.1186/s13287-017-0694-z https://stemcellres.biomedcentral.com/track/pdf/10.1186/s13287-017-0694-z

[2] Chen YJ, Finkbeiner SR, Weinblatt D, Emmett MJ, Tameire F, Yousefi M, Yang C, Maehr R, Zhou Q, Shemer R, Dor Y, Li C, Spence JR, Stanger BZ. De novo formation of insulin-producing "neo-β cell islets" from intestinal crypts. Cell Rep. 2014 Mar 27;6(6):1046-1058. doi: 10.1016/j.celrep.2014.02.013. Epub 2014 Mar 6. PMID: 24613355; PMCID: PMC4245054. https://pubmed.ncbi.nlm.nih.gov/24613355/

[3] Wang H, Brun T, Kataoka K, Sharma AJ, Wollheim CB. MAFA controls genes implicated in insulin biosynthesis and secretion. Diabetologia. 2007;50(2):348-358. doi:10.1007/s00125-006-0490-2 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2196442/