Difference between revisions of "Part:BBa K3450005"
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| − | + | 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] | ||
| + | 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/ | ||
Revision as of 17:35, 23 October 2020
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] 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/