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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 38 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 7 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 (显示 INS 抗体)-producing cells in vivo by transfection of neurogenin-3 (显示 NEUROG3 抗体), Pdx1 (显示 PDX1 抗体), 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 (显示 PDX1 抗体) = pancreatic and duodenal homeobox 1 (显示 PDX1 抗体); MafA = v-maf (显示 MAF 抗体) musculoaponeurotic fibrosarcoma oncogene (显示 RAB1A 抗体) family, protein A (显示 GPR153 抗体))
Treg cell accumulation in intestinal tumours from APC (显示 APC 抗体)(min/+) mice was exclusively due to the increase in KLRG1 (显示 KLRG1 抗体)(+) GATA3 (显示 GATA3 抗体)(+) Treg cells.
Although absence of KLRG1 (显示 KLRG1 抗体) is not enough to increase intestinal Treg cells in KLRG1 (显示 KLRG1 抗体) knockout mice, KLRG1 (显示 KLRG1 抗体) ligation reduces T-cell receptor signals and the competitive fitness of individual Treg cells in the intestine.
Mafa was found to both potentiate the ability of Pdx1 (显示 PDX1 抗体) to induce beta-cell formation from Ngn3 (显示 NEUROG3 抗体)-positive endocrine precursors and enable Pdx1 (显示 PDX1 抗体) to produce beta-cells from alpha-cells.
Ly6C, 4-1BB (显示 TNFRSF9 抗体), and KLRG1 (显示 KLRG1 抗体) have roles in the activation of lamina propria lymphocytes in the small intestine in a mouse model of Crohn's disease
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 (显示 MAO 抗体) activity in beta cells is pivotal for physiological insulin (显示 INS 抗体) secretion and that loss of MaoB (显示 MAOB 抗体) expression may contribute to the beta cell dysfunction in type 2 diabetes.
is necessary for the maintenance of normal insulin (显示 INS 抗体) levels even in embryos.
endogenous small-Maf (显示 MAF 抗体) factors negatively regulate beta-cell function by competing for MafA binding, and thus, the inhibition of small-Maf (显示 MAF 抗体) activity can improve beta-cell function
Data, including data from studies using transgenic/knockout mice, confirm the expression of Mafa and Mafb (显示 MAFB 抗体) is specific to insulin (显示 INS 抗体)-secreting cells of the pancreas.
Pdx1 (显示 PDX1 抗体) and MafA (显示 KLRG1 抗体) play crucial roles in the pancreas and maintain mature beta-cell function. Our results showed that the expression of Pdx1 (显示 PDX1 抗体) and MafA (显示 KLRG1 抗体) 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.
MAFA (显示 KLRG1 抗体), MAFB (显示 MAFB 抗体), NKX6.1 (显示 NKX6-1 抗体), and PDX1 (显示 PDX1 抗体) activity provides a gauge of islet beta cell function, with loss of MAFA (显示 KLRG1 抗体) (and/or MAFB (显示 MAFB 抗体)) representing an early indicator of beta cell inactivity
Loss of MAFA (显示 KLRG1 抗体) expression is associated with insulinoma (显示 RPS15 抗体).
MAFA (显示 KLRG1 抗体) nuclear expression in pancreatic alpha and beta cells, and the percentage of alpha cells expressing PAX4 (显示 PAX4 抗体) are altered in patients with type 2 diabetes.
under oxidative and nonoxidative conditions p38 MAPK (显示 MAPK14 抗体) directly binds to MafA (显示 KLRG1 抗体) and triggers MafA (显示 KLRG1 抗体) degradation via ubiquitin proteasomal pathway.
Beta cell nuclear MafA (显示 KLRG1 抗体) 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 (显示 PDX1 抗体), NeuroD1 (显示 NEUROD1 抗体), and MafA (显示 KLRG1 抗体), causes differentiation of bone marrow mesenchymal stem cells into insulin (显示 INS 抗体)-producing cells
Data suggest that MafA (显示 KLRG1 抗体) 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.
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
, macrophage/microglia activation-associated factor
, monocyte to macrophage differentiation factor
, monocyte to macrophage differentiation protein
, progestin and adipoQ receptor family member XI
, LOW QUALITY PROTEIN: transcription factor MafA
, v-maf avian musculoaponeurotic fibrosarcoma oncogene homolog A