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confirm the association of miR-204 with a beta cell endocrine phenotype in human pancreatic islets, but do not support its direct role in regulating the levels of insulin mRNA through MAFA
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We investigated a large pedigree with autosomal dominant inheritance of diabetes mellitus or insulinomatosis, an adult-onset condition of recurrent hyperinsulinemic hypoglycemia caused by multiple insulin-secreting neuroendocrine tumors of the pancreas. Using exome sequencing, we identified a missense MAFA mutation (p.Ser64Phe, c.191C>T) segregating with both phenotypes of insulinomatosis and diabetes.
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PDX1, Neurogenin-3, and MAFA are critical transcription regulators for beta cell development and regeneration. (Review)
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USP5 regulates c-Maf stability and multiple myeloma cell survival.
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Pdx1 and MafA play crucial roles in the pancreas and maintain mature beta-cell function. Our results showed that the expression of Pdx1 and MafA were significantly upregulated after a sleeve gastrectomy for morbid obesity.
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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 patients with 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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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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Loss of MAFA expression is associated with insulinoma.
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MAFA nuclear expression in pancreatic alpha and beta cells, and the percentage of alpha cells expressing PAX4 are altered in patients with type 2 diabetes.
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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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Beta cell nuclear MafA is markedly decreased in humans with type 2 diabetes, which may contribute to impaired beta cell dysfunction.
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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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Data suggest that MafA plays a novel role in the reprogramming of stem cells into pancreatic beta-progenitors, promotes the islet-like characteristics of PDMSCs, as well as functionally regulation of blood glucose levels in transplanted grafts.
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ATF2 interacts with beta-cell-enriched transcription factors, MafA, Pdx1, and beta2, and activates insulin gene transcription.
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MafA transcription is upregulated in beta-cells acutely cultured in high glucose similar to what may occur in vivo under normoglycemic conditions.
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a novel relationship between the phosphoamino acid-rich transactivation and b-Zip domains in controlling MafA DNA-binding activity.
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In addition to its expression in pancreatic beta cells, MafA also identifies the early ret-expressing sensory neurons in the dorsal root ganglia.
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gene is unlikely to have a significant role in monogenic diabetes in humans
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MafA selectively induces endogenous insulin transcription in non-beta cells