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Data suggest that hepatocytes can be reprogrammed into insulin-producing cells in vivo by transfection of neurogenin-3, Pdx1, and MafA genes using non-viral hydrodynamics injection; this procedure was used in treatment of streptozotocin diabetes; fasting blood glucose was reduced to normal. (Pdx1 = pancreatic and duodenal homeobox 1; MafA = v-maf musculoaponeurotic fibrosarcoma oncogene family, protein A)
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Mafa was found to both potentiate the ability of Pdx1 to induce beta-cell formation from Ngn3-positive endocrine precursors and enable Pdx1 to produce beta-cells from alpha-cells.
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MAFA controls autonomic nervous system-mediated insulin secretion by activating the transcription of nicotinic (ChrnB2 and ChrnB4) receptor genes, which is impaired in type 2 diabetes.
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These findings demonstrate that regulation of monoamine levels by Mao activity in beta cells is pivotal for physiological insulin secretion and that loss of MaoB expression may contribute to the beta cell dysfunction in type 2 diabetes.
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is necessary for the maintenance of normal insulin levels even in embryos.
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endogenous small-Maf factors negatively regulate beta-cell function by competing for MafA binding, and thus, the inhibition of small-Maf activity can improve beta-cell function
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Data, including data from studies using transgenic/knockout mice, confirm the expression of Mafa and Mafb is specific to insulin-secreting cells of the pancreas.
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These results suggest that MafA regulates the postnatal proliferation of beta-cells via prolactin signaling.
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results illustrate how consequential the reduction in Mafa activity is to islet beta-cell function under pathophysiological conditions.
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Results not only clearly define why MafA is an essential transcriptional regulator of islet beta-cells, but also why cell maturation involves coordinated actions with MafB.
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MAFA, MAFB, NKX6.1, and PDX1 activity provides a gauge of islet beta cell function, with loss of MAFA (and/or MAFB) representing an early indicator of beta cell inactivity
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under oxidative and nonoxidative conditions p38 MAPK directly binds to MafA and triggers MafA degradation via ubiquitin proteasomal pathway.
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In this study, we tried to establish an effective method of differentiation through the protein transduction of three transcription factors (Pdx1, NeuroD, and MafA) important to pancreatic beta cell development.
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We found that forcing MafA transgene expression, out of its normal developmental context, in Ngn3(+) endocrine progenitors blocked endocrine differentiation and prevented the formation of hormone(+) cells.
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We identified MAFA as a target that is downregulated by miR-204. The newly identified TXNIP-miR-204-MAFA-insulin pathway may contribute to diabetes progression.
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Findings suggest that Onecut1 suppresses MafA gene expression through the Foxa2-binding site.
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Characterization of an apparently novel beta-cell line-enriched 80-88 kDa transcriptional activator of the MafA and Pdx1 genes.
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MicroRNA-30d induces insulin transcription factor MafA and insulin production by targeting mitogen-activated protein 4 kinase 4 (MAP4K4) in pancreatic beta-cells.
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Combined transfection of the three transcriptional factors, PDX-1, NeuroD1, and MafA, causes differentiation of bone marrow mesenchymal stem cells into insulin-producing cells
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Results indicate that Pdx1 and MafA drive DE progenitors towards insulin-producing cells.
