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The protein encoded by NEUROG3 is a basic helix-loop-helix (bHLH) transcription factor involved in neurogenesis. Zusätzlich bieten wir Ihnen Neurogenin 3 Antikörper (112) und Neurogenin 3 Proteine (6) und viele weitere Produktgruppen zu diesem Protein an.
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These results provide new detail regarding the Ngn3 transcriptional network operating in endocrine progenitor cells to specify a beta (zeige SUCLA2 ELISA Kits) cell phenotype
Sox9 (zeige SOX9 ELISA Kits) and Ngn3, key transcription factors associated with pancreatic development.
This reviews the expression and function of NEUROG3 in both mouse and human pancreatic development. [Review Article]
Neurogenin3 controls its ability to promote pancreatic endocrine differentiation and to maintain beta cell function in the presence of pro-proliferation cues
Phosphorylation of NEUROG3 links endocrine differentiation to the cell cycle in pancreatic progenitors
Collectively, our results demonstrate that the STAT3 (zeige STAT3 ELISA Kits)(K392R) mutation causes premature endocrine differentiation through direct induction of NEUROG3 expression.
inflammatory cytokine insults stimulate epithelial-to-mesenchymal transition (EMT (zeige ITK ELISA Kits)) as well as the endocrine program in human pancreatic ductal cells via STAT3 (zeige STAT3 ELISA Kits)-dependent NGN3 activation.
ChIP experiments confirmed that Pdx1 (zeige PDX1 ELISA Kits) activates the expression of the downstream transcription factors, Ngn3 and Pax6 (zeige PAX6 ELISA Kits), by combined with the promoter regions of insulin (Insulin (zeige INS ELISA Kits)-P), Ngn3 (Ngn3-P), and Pax6 (Pax6 (zeige PAX6 ELISA Kits)-P).
NGN3 expression in the adult human exocrine pancreas marks a dedifferentiating cell population.
conclude that NEUROG3 is essential for endocrine pancreas development in humans and that as little as 10% NEUROG3 is sufficient for formation of pancreatic endocrine cells
NEUROG3 deficiency produces a rare clinical syndrome characterised by severe malabsorptive diarrhoea from early life and mild diabetes with a variable age of onset.
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)
limiting Neurog3 expression dramatically increased the proportional representation of Sox9 (zeige SOX9 ELISA Kits)(+) Neurog3(TA.LO) progenitors, with a doubling of its mitotic index relative to normal Neurog3 expression, suggesting that low Neurog3 expression is a defining feature of this cycling endocrine-biased state
Duplication of pre-existing beta-cells is not the sole source of new beta-cells during pregnancy; Ngn3 may be involved in this process.
data demonstrate that HIF1-alpha (zeige HIF1A ELISA Kits) negatively controls beta cell differentiation in vivo by regulating NGN3 expression, and that this effect is mediated by signals from blood vessels.
Data indicate that all neurogenin 3 (Neurog3)-tuberous sclerosis complex 1 (Tsc1 (zeige TSC1 ELISA Kits))-/- mice developed notable adenocarcinoma-like lesions in pancreas starting from the age of 100 days old.
Activation of the developmental pathway neurogenin-3/microRNA-7a regulates cholangiocyte proliferation in response to injury.
The control of endocrine cell fate is instead fulfilled by two basic helix-loop-helix factors, Ascl1b and Neurod1 (zeige NEUROD1 ELISA Kits) and NEUROG3 is not the unique pancreatic endocrine cell fate determinant in vertebrates.
Nkx2.2 coordinately activates NeuroD1 with Ngn3 in the endocrine progenitor cell and plays a role in the maintenance of NeuroD1 expression to regulate beta cell function in the mature islet.
The protein encoded by this gene is a basic helix-loop-helix (bHLH) transcription factor involved in neurogenesis. The encoded protein likely acts as a heterodimer with another bHLH protein. Defects in this gene are a cause of congenital malabsorptive diarrhea 4 (DIAR4).
, class A basic helix-loop-helix protein 7
, protein atonal homolog 5
, Neurogenin 3 (Atonal protein homolog 5) (Helix-loop-helix protein mATH-4B) (MATH4B)
, atonal homolog 5
, helix-loop-helix protein mATH-4B
, transcriptional regulator, Relax
, atonal homolog 4