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Human Polyclonal MAFA Primary Antibody for ChIP, GS - ABIN152904
Wang, Torres-Gonzalez, Tripathy, Botolin, Christian, Jump: Elevated hepatic fatty acid elongase-5 activity affects multiple pathways controlling hepatic lipid and carbohydrate composition. in Journal of lipid research 2008
Show all 40 Pubmed References
Human Polyclonal MAFA Primary Antibody for ICC, IF - ABIN4332350
Raum, Hunter, Artner, Henderson, Guo, Elghazi, Sosa-Pineda, Ogihara, Mirmira, Sussel, Stein: Islet beta-cell-specific MafA transcription requires the 5'-flanking conserved region 3 control domain. in Molecular and cellular biology 2010
Show all 11 Pubmed References
Human Polyclonal MAFA Primary Antibody for WB - ABIN4332352
Brundage, Tandon, Eaves, Williams, Miller, Hennigan, Jegga, Cripe, Ratner: MAF mediates crosstalk between Ras-MAPK and mTOR signaling in NF1. in Oncogene 2014
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)
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.
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.
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.
is necessary for the maintenance of normal insulin levels even in embryos.
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
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.
These results suggest that MafA regulates the postnatal proliferation of beta-cells via prolactin signaling.
results illustrate how consequential the reduction in Mafa activity is to islet beta-cell function under pathophysiological conditions.
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.
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
under oxidative and nonoxidative conditions p38 MAPK directly binds to MafA and triggers MafA degradation via ubiquitin proteasomal pathway.
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.
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.
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.
Findings suggest that Onecut1 suppresses MafA gene expression through the Foxa2-binding site.
Characterization of an apparently novel beta-cell line-enriched 80-88 kDa transcriptional activator of the MafA and Pdx1 genes.
MicroRNA-30d induces insulin transcription factor MafA and insulin production by targeting mitogen-activated protein 4 kinase 4 (MAP4K4) in pancreatic beta-cells.
Combined transfection of the three transcriptional factors, PDX-1, NeuroD1, and MafA, causes differentiation of bone marrow mesenchymal stem cells into insulin-producing cells
Results indicate that Pdx1 and MafA drive DE progenitors towards insulin-producing cells.
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
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.
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.
Beta cell nuclear MafA is markedly decreased in humans with type 2 diabetes, which may contribute to impaired beta cell dysfunction.
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
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