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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.
PDX1, Neurogenin-3, and MAFA are critical transcription regulators for beta cell development and regeneration. (Review)
USP5 regulates c-Maf stability and multiple myeloma cell survival.
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.
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.
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.
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
Loss of MAFA expression is associated with insulinoma.
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.
under oxidative and nonoxidative conditions p38 MAPK directly binds to MafA and triggers MafA degradation via ubiquitin proteasomal pathway.
Beta cell nuclear MafA is markedly decreased in humans with type 2 diabetes, which may contribute to impaired beta cell dysfunction.
Combined transfection of the three transcriptional factors, PDX-1, NeuroD1, and MafA, causes differentiation of bone marrow mesenchymal stem cells into insulin-producing cells
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.
ATF2 interacts with beta-cell-enriched transcription factors, MafA, Pdx1, and beta2, and activates insulin gene transcription.
MafA transcription is upregulated in beta-cells acutely cultured in high glucose similar to what may occur in vivo under normoglycemic conditions.
a novel relationship between the phosphoamino acid-rich transactivation and b-Zip domains in controlling MafA DNA-binding activity.
In addition to its expression in pancreatic beta cells, MafA also identifies the early ret-expressing sensory neurons in the dorsal root ganglia.
gene is unlikely to have a significant role in monogenic diabetes in humans
MafA selectively induces endogenous insulin transcription in non-beta cells
mafA has a role in regulating insulin gene expression in the liver
Report pancreatic expression of MafA in pancreas.
MAFA is a transcription factor that binds RIPE3b, a conserved enhancer element that regulates pancreatic beta cell-specific expression of the insulin gene (INS\; MIM 176730) (Olbrot et al., 2002
, V-maf musculoaponeurotic fibrosarcoma oncogene homolog A
, pancreatic beta-cell-specific transcriptional activator
, transcription factor MafA
, transcription factor RIPE3b1
, v-maf musculoaponeurotic fibrosarcoma oncogene family, protein A
, v-maf musculoaponeurotic fibrosarcoma oncogene homolog A
, Transcription factor MafA
, leucine zipper transcription factor
, somite Maf1
, v-maf musculoaponeurotic fibrosarcoma oncogene family, protein L
, bZIP transcription factor L-Maf
, lens-specific Maf
, LOW QUALITY PROTEIN: transcription factor MafA
, v-maf avian musculoaponeurotic fibrosarcoma oncogene homolog A