Topic
NeuroD
About: NeuroD is a research topic. Over the lifetime, 545 publications have been published within this topic receiving 39105 citations.
Papers published on a yearly basis
Papers
TL;DR: Ngn3 is required for the specification of a common precursor for the four pancreatic endocrine cell types, and it is shown that ngn3-positive cells coexpress neither insulin nor glucagon, suggesting thatngn3 marks early precursors of pancreaticendocrine cells.
Abstract: In the mammalian pancreas, the endocrine cell types of the islets of Langerhans, including the α-, β-, δ-, and pancreatic polypeptide cells as well as the exocrine cells, derive from foregut endodermal progenitors. Recent genetic studies have identified a network of transcription factors, including Pdx1, Isl1, Pax4, Pax6, NeuroD, Nkx2.2, and Hlxb9, regulating the development of islet cells at different stages, but the molecular mechanisms controlling the specification of pancreatic endocrine precursors remain unknown. neurogenin3 (ngn3) is a member of a family of basic helix–loop–helix transcription factors that is involved in the determination of neural precursor cells in the neuroectoderm. ngn3 is expressed in discrete regions of the nervous system and in scattered cells in the embryonic pancreas. We show herein that ngn3-positive cells coexpress neither insulin nor glucagon, suggesting that ngn3 marks early precursors of pancreatic endocrine cells. Mice lacking ngn3 function fail to generate any pancreatic endocrine cells and die postnatally from diabetes. Expression of Isl1, Pax4, Pax6, and NeuroD is lost, and endocrine precursors are lacking in the mutant pancreatic epithelium. Thus, ngn3 is required for the specification of a common precursor for the four pancreatic endocrine cell types.
1,550 citations
TL;DR: It appears that GABAergic inputs to hippocampal progenitor cells promote activity-dependent neuronal differentiation through the promotion of neuronal differentiation via this GABAergic excitation.
781 citations
TL;DR: These data and those of Fode et al. (1998 [this issue of Neuron]) identify ngns as vertebrate neuronal determination genes, analogous to myoD and myf5 in myogenesis.
760 citations
TL;DR: It is demonstrated that excitatory stimuli act directly on adult hippocampal NPCs to favor neuron production and, when applied as an "excitation-neurogenesis coupling rule", predict significant advantages for both the temporary storage and the clearance of memories.
740 citations
TL;DR: These findings suggest that deficient binding of NEUROD1 or binding of a transcriptionally inactive NEurOD1 polypeptide to target promoters in pancreatic islets leads to the development of type 2 diabetes in humans.
Abstract: The helix-loop-helix (HLH) protein NEUROD1 (also known as BETA2) functions as a regulatory switch for endocrine pancreatic development. In mice homozygous for a targeted disruption of Neurod, pancreatic islet morphogenesis is abnormal and overt diabetes develops due in part to inadequate expression of the insulin gene (Ins2). NEUROD1, following its heterodimerization with the ubiquitous HLH protein E47, regulates insulin gene (INS) expression by binding to a critical E-box motif on the INS promoter. Here we describe two mutations in NEUROD1, which are associated with the development of type 2 diabetes in the heterozygous state. The first, a missense mutation at Arg 111 in the DNA-binding domain, abolishes E-box binding activity of NEUROD1. The second mutation gives rise to a truncated polypeptide lacking the carboxy-terminal trans-activation domain, a region that associates with the co-activators CBP and p300 (refs 3,4). The clinical profile of patients with the truncated NEUROD1 polypeptide is more severe than that of patients with the Arg 111 mutation. Our findings suggest that deficient binding of NEUROD1 or binding of a transcriptionally inactive NEUROD1 polypeptide to target promoters in pancreatic islets leads to the development of type 2 diabetes in humans.
640 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2025 | 13 |
| 2024 | 40 |
| 2023 | 10 |
| 2022 | 34 |
| 2021 | 13 |
| 2020 | 14 |