Ask about this productRelated genes to: NEUROG1 antibody
- Gene:
- NEUROG1 NIH gene
- Name:
- neurogenin 1
- Previous symbol:
- NEUROD3
- Synonyms:
- AKA, Math4C, ngn1, bHLHa6
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-10
- Date modifiied:
- 2016-10-05
Related products to: NEUROG1 antibody
Related articles to: NEUROG1 antibody
- Prenatal exposure to opioids such as morphine poses significant risks to fetal neurodevelopment, particularly in brain regions critical for cognition, such as the hippocampus. Despite the prescription and use of opioids during pregnancy, the molecular and histological consequences of such exposure remain insufficiently explored. To evaluate the effects of short-term prenatal morphine exposure on the expression of key neurodevelopmental genes and the structural integrity of the hippocampus in neonatal rats. - Source: PubMed
Nadri PooyaDaneshfar ZahraAzarmehr ZahraFarrokhfar Samaneh - VESTIGIAL-LIKE proteins constitute a family of evolutionarily conserved proteins that act as cofactors in regulating gene expression through their binding to TEAD transcription factors. Among the four members of this family in vertebrates, VESTIGIAL-LIKE 4 has emerged as a tumor suppressor that competes with YAP in binding TEADs, thus inhibiting the HIPPO pathway downstream of YAP. Nevertheless, very few studies have addressed its function during early vertebrate development. Here, we used gain- and loss-of-function strategies to investigate the role of vestigial-like 4 during development. Our data show that vestigial-like 4 is a key regulator of neurogenesis and neural crest formation. In embryos depleted of vestigial-like 4, neurogenesis is severely impaired, and neither neurog1 nor neurod1 is able to stimulate neurogenesis. Vestigial-like 4 is also required for neural crest formation through and sox9 regulation, and this property does not necessarily require its interaction with tead. Collectively, our findings demonstrate that vestigial-like 4 is an important regulator of neurogenesis and neural crest formation. Although vestigial-like 4 can bind to tead proteins in the embryo, its function does not depend solely on this interaction, suggesting a complex level of regulation with which vestigial-like 4 regulates early steps in development and differentiation. - Source: PubMed
Publication date: 2026/02/11
Thiébaud PierreSimon EmilieMoisan FrançoisFedou SandrineRezvani Hamid-RezaThézé Nadine - Dorsal root ganglia (DRG) somatosensory neurons of the mechano/proprioceptive and thermo/nociceptive lineages differentiate during successive neurogenic waves defined by the complementary expression and combinatorial roles of the proneural genes Neurog2 and Neurog1. Using a gene-swapping approach, we show here that both paralogs are largely interchangeable in this structure and beyond, including for fate determination, indicating that their specific requirements primarily reflect divergent evolution of their regulatory sequences rather than protein activities. This result, combined with birth-dating data and phenotyping of complementary transgenic models, where delayed onset or premature arrest of neurogenesis predictably triggers opposite changes in DRG content, highlights that somatosensory precursors' commitment to the mechano/proprioceptive or thermo/nociceptive lineage is rapidly biased but critically depends on differentiation timing. Together, these findings support a model where the dynamic spatiotemporal expression of functionally equivalent Neurog1 and Neurog2 proteins ensures a protracted neurogenic period, allowing the sequential emergence of distinct neuronal lineages. - Source: PubMed
Publication date: 2026/01/13
Desiderio SimonCabochette PaulineVenteo StephanieTejedor GautierDjouad FaridaCarroll PatrickAngo FabricePattyn Alexandre - Vestibular and spiral ganglion neurons (VGNs and SGNs) developed in the inner ear, where they extend fibers to innervate the vestibular and cochlear hair cells and project centrally to the vestibular and cochlear nuclei. This review focuses on representative molecular factors that regulate key processes in the development of inner ear neurons, including their specification, differentiation, axon targeting, and functional diversification. A temporal regulatory cascade defines the initial precursors through factors such as Smarca4, Six1, Eya1, followed by Sox2. While Sox2 deletion abolishes hair cell formation, a subset of inner ear neurons transiently develops but undergoes apoptosis before birth. In contrast, Neurog1 deletion eliminates all ear-derived neurons but results in differential reductions in cochlear and vestibular hair cells. The development and survival of inner ear neurons depend on TrkB and TrkC signaling. Although deletion of TrkB and TrkC results in a complete loss of neurons, each shows distinct effects on VGN and SGN survival and innervation. Downstream of early transcriptional regulators, Neurod1 and Isl1 promote neuronal differentiation, survival, migration, and the formation of peripheral and central projections. The development of VGNs depends on at least two progenitor populations that give rise to three neuronal subtypes that differ in their innervation of vestibular hair cells but show incomplete segregation in the vestibular nuclei. In contrast, SGNs develop later and exhibit sequential segregation into four neuronal subtypes, corresponding to the two types of cochlear hair cells, with tonotopically organized projections to both the cochlea and cochlear nuclei. - Source: PubMed
Publication date: 2026/01/05
Pavlinkova GabrielaXu Pin-XianCheah Kathryn S EYamoah Ebenezer NFritzsch Bernd - The basic helix-loop-helix transcription factors, Neurog1 and Neurod1, orchestrate spiral ganglion neuron (SGN) differentiation in the embryonic cochlea. Their knockout leads to profound SGN and hair cell (HC) loss, cochlear truncation, and hearing impairment. To investigate SGN diversification and lineage origins, we generated three knock-in mouse strains: Neurod1-Cre, Neurod1-iCreER, and Neurog1-iCreER. In Neurod1-Cre; Rosa26-LSL-tdTomato (Ai9) mice, in addition to SGNs, tdTomato HCs and supporting cells were observed, displaying an apical-to-basal gradient. Tamoxifen induction at embryonic day 7.5 (E7.5) also labeled HCs in Neurog1-iCreER/iCreER; Ai9/+ mice at E18.5. Notably, a pure population of SGNs was traced in Neurod1-iCreER/+; Ai9/+ mice with tamoxifen administration from E7.5 to postnatal day 0 (P0). Dose standardization further enabled maximal SGN labeling upon induction at E12.5. These results illuminate the progenitor origins and developmental trajectories of SGNs and HCs, and establish a functional genetic tool for sorting and conditional manipulation of SGNs in auditory research. - Source: PubMed
Publication date: 2025/12/27
Chen ZhijiZhou XiaoqingYang TingLiu XuelaiZhang JuhongFeng MenglongKuang ShaojingYuan Wei