Disease relevance of Neurod1

• Transfection of the NeuroD-expression plasmid into PC12 cells, a rat pheochromocytoma cell line, induced morphological changes featured by neurite-like processes and synapse-like structures without a differentiation-inducing reagent such as NGF [1].
• A basic helix-loop-helix transcription factor NeuroD at 7 and 14 days and an immature migrating neuronal marker doublecortin at 14 days after ischemia were expressed transiently in proliferative cells [2].
• These results indicate that BETA2/NeuroD plays an important role in terminal differentiation of neuroblastoma cells [3].

Psychiatry related information on Neurod1

• In conclusion, our results indicate that thyroid hormones (TH) regulate the expression of NeuroD during the "critical period" of cerebellum development [4].

High impact information on Neurod1

• These findings uncover an essential function for NeuroD in granule neuron dendritic morphogenesis [5].
• We found that the genetic knockdown of the transcription factor NeuroD in primary granule neurons including in organotypic cerebellar slices profoundly impaired the generation and maintenance of dendrites while sparing the development of axons [5].
• Mammalian hairy and Enhancer of split homolog 1 (HES1), a basic helix-loop-helix factor gene, is expressed in retinal progenitor cells, and its expression decreases as differentiation proceeds [6].
• The present study provides evidence that the homeodomain of PDX-1 acts as a protein-protein interaction domain to recruit multiple proteins, including E47/Pan1, BETA2/NeuroD1, and high-mobility group protein I(Y), to an activation complex on the E2A3/4 minienhancer [7].
• In support of this, we show that ATBF1 suppresses nestin expression, a neural stem cell marker, and activates the promoter of Neurod1 gene, a marker for neuronal differentiation [8].

Biological context of Neurod1

• In conclusion, increased expression of c-Myc in beta-cells suppresses the insulin gene transcription by inhibiting NeuroD-mediated transcriptional activation [9].
• Treatment with the MEK inhibitor PD98059 or substitution of a serine for an alanine at a potential mitogen-activated protein kinase phosphorylation site (S274) in NeuroD1 significantly increased the cytoplasmic level at 20 mM glucose [10].
• Electrophoretic mobility shift assays demonstrated that NeuroD was able to interact with a proximal E-box element of the AK1 promoter [1].
• The CAT reporter assay of the 5'-flanking region of the AK1 gene suggests that NeuroD activates the AK1 expression through E-boxes in the promoter region [1].
• Assignment of Neurod1 to rat chromosome 3 band 3q24-->q32 and mouse chromosome 2 band 2E2-E3 by in situ hybridization [11].

Anatomical context of Neurod1

• Association with the nuclear matrix and interaction with Groucho and RUNX proteins regulate the transcription repression activity of the basic helix loop helix factor Hes1 [12].
• Overexpression of BETA2/NeuroD induces neurite outgrowth in F11 neuroblastoma cells [3].
• BETA2/NeuroD, a basic helix-loop-helix (bHLH) transcription factor, has been shown to play important roles in the development of the nervous system and the maintenance and formation of pancreatic and enteroendocrine cells [3].
• The neurogenic basic helix-loop-helix transcription factor NeuroD protein in the dentate gyrus after MK-801 treatment was expressed transiently in proliferative cells, but not in mature neurons [13].
• One day after the injection, BrdU-labeled cells were found frequently in clusters consisting of dividing cells, putative undifferentiated cells, NeuroD-positive differentiated neurons, and GFAP-positive astrocytes [14].

Associations of Neurod1 with chemical compounds

• The rise in NeuroD1-mediated transcription in response to glucose also correlated with the change in sub-cellular localization, a response attenuated by PD98059 [10].
• Thyroid hormone regulates the expression of NeuroD/BHF1 during the development of rat cerebellum [4].
• The expressions of NeuroD, BDNF, and NR1 mRNA levels and protein levels of p-ERK and p-CREB were remarkably decreased by corticosterone in a dose-dependent manner [15].

Regulatory relationships of Neurod1

• Overexpression of NeuroD in PC12 cells alters morphology and enhances expression of the adenylate kinase isozyme 1 gene [1].

Other interactions of Neurod1

• The numbers of basal cells expressing the proneural transcriptional activators Mash1, Neurogenin1, and NeuroD all fall precipitously 1 day after lesion [16].
• Together, these findings establish the novel calbindin-regulated function of CaMKII and NeuroD in control of neuronal differentiation and neurite outgrowth [17].
• Adult and embryonic progenitors commonly expressed various homeodomain-type (Pax6, Pax7, Nkx2.2, and Prox1) and basic helix-loop-helix (bHLH)-type (Ngn2, Mash1, NeuroD1, and Olig2) transcriptional regulatory factors in vitro [18].
• After terminal differentiation, granule cells born in the hilus or the subgranular zone begin to express NeuroD followed by NeuroD2 [19].
• In this study, we investigated the neurogenic potential of BETA2/NeuroD using neuroblastoma cell line, F11, which could be induced to differentiate into neurons in the presence of cAMP [3].

Analytical, diagnostic and therapeutic context of Neurod1

• A rat NeuroD cDNA was obtained by the aid of reverse transcription-polymerase chain reaction (RT-PCR) and ligated to an expression vector having a CMV promoter [1].
• Expression of MASH-1, NeuroD, NeuroD-related factor (NDRF) and HES-1 was demonstrated in HC2S2 cells by Northern blot analysis using total RNA [20].

References