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The protein encoded by NEUROG3 is a basic helix-loop-helix (bHLH) transcription factor involved in neurogenesis. Additionally we are shipping Neurogenin 3 Antibodies (114) and Neurogenin 3 Kits (5) and many more products for this protein.
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These results provide new detail regarding the Ngn3 transcriptional network operating in endocrine progenitor cells to specify a beta (show SUCLA2 Proteins) cell phenotype
Collectively, our results demonstrate that the STAT3 (show STAT3 Proteins)(K392R) mutation causes premature endocrine differentiation through direct induction of NEUROG3 expression.
inflammatory cytokine insults stimulate epithelial-to-mesenchymal transition (EMT (show ITK Proteins)) as well as the endocrine program in human pancreatic ductal cells via STAT3 (show STAT3 Proteins)-dependent NGN3 activation.
ChIP experiments confirmed that Pdx1 (show PDX1 Proteins) activates the expression of the downstream transcription factors, Ngn3 and Pax6 (show PAX6 Proteins), by combined with the promoter regions of insulin (Insulin (show INS Proteins)-P), Ngn3 (Ngn3-P), and Pax6 (Pax6 (show PAX6 Proteins)-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.
Activation of the developmental pathway neurogenin-3/microRNA-7a regulates cholangiocyte proliferation in response to injury.
The expression of transcription factor Ngn3 and pancreatic mesenchymal microenvironment are important and necessary to promote pancreatic progenitors differentiated to islet cells regardless of pancreatic development or islets regeneration.
Recessively inherited NEUROG-3 mutations were originally identified in three patients with unexplained congenital malabsorptive diarrhea and an absence of EC.
Prospectively isolated NGN3-expressing progenitors from human embryonic stem cells give rise to pancreatic endocrine cells.
limiting Neurog3 expression dramatically increased the proportional representation of Sox9 (show SOX9 Proteins)(+) 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 (show HIF1A Proteins) 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 (show TSC1 Proteins))-/- mice developed notable adenocarcinoma-like lesions in pancreas starting from the age of 100 days old.
Hnf1b plays a crucial role in the regulatory networks that control pancreatic MPC expansion, acinar cell identity, duct morphogenesis and generation of endocrine precursors.
The role of neurogenin 3 and PD-L1 (show CD274 Proteins) in the genesis of neo-islets in NOD mice is reported.
Neurog3 establishes the posterior boundary of the serotonergic system by actively suppressing serotonergic specification in the spinal cord.
Insm1 (show INSM1 Proteins) works to promote endocrine cell differentiation in a pathway that involves Neurog3 and Ripply3 (show DSCR6 Proteins)
The control of endocrine cell fate is instead fulfilled by two basic helix-loop-helix factors, Ascl1b and Neurod1 (show NEUROD1 Proteins) 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