NEUROG1 antibody - C-terminal region (ARP32038_P050)
- Known as:
- NEUROG1 (anti-) - C-terminal region (ARP32038_P050)
- Catalog number:
- arp32038_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- NEUROG1 antibody - C-terminal region (ARP32038_P050)
Related genes to: NEUROG1 antibody - C-terminal region (ARP32038_P050)
- 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 - C-terminal region (ARP32038_P050)
Related articles to: NEUROG1 antibody - C-terminal region (ARP32038_P050)
- Olfactory dysfunction is a debilitating condition with no established treatment. This study evaluated the efficacy of intranasal (i.n.) NAD administration in restoring olfactory function. Cultured human olfactory stem cells (hOSCs) were treated with NAD and assessed by immunofluorescence staining, PCR, and western blot analyses. In vivo, mice with ZnSO-induced anosmia were treated with i.n. NAD, intraperitoneal dexamethasone, or PBS and evaluated by histological analysis, behavioral tests, bulk RNA-sequencing (RNA-seq), and in situ hybridization. NAD promoted hOSC differentiation into olfactory sensory neurons (OSNs), evidenced by increased stem cell (SOX2 and nestin) and OSN markers (Tuj1 and OMP) expression, and upregulated neuronal differentiation-related genes (SOX2, NESTIN, NEUROD1, NEUROG1, and OMP). In vivo, the NAD group showed significant olfactory function improvement and marked olfactory epithelium repair. Bulk RNA-seq of the olfactory turbinate tissue identified 113 differentially expressed genes (cluster T1) upregulated in control and NAD groups. The Gene Ontology (GO) term "modulation of chemical synaptic transmission" was associated with cluster T1, and 25 genes implicated in this GO were upregulated in the NAD group. Integration with publicly available single-cell RNA-seq data identified six neuronal marker genes - ABHD2, DLGAP2, FOXO3, HIPK2, KCNMA1, and PCDH17 - upregulated by NAD. Protein expression of DLGAP2 and PCDH17 was higher in differentiated hOSCs treated with NAD. In situ hybridization confirmed that Dlgap2, Foxo3, and Pcdh17 expression was restored in anosmic mice treated with i.n. NAD. The potential therapeutic efficacy of i.n. NAD administration was demonstrated by showing regeneration of OSNs in hOSCs and restoring olfactory function in an anosmia mouse model. - Source: PubMed
Publication date: 2026/07/01
Yoo Shin HyukJang Jung YeonBae Jun-SangVentura ReizaKim Eun HeeKim A YoungMo Ji-HunPark JaewooKang KyuhoYun YeogyunLee Jun HeeKim Yong-JaeLee Dong-JoonKim Ji Heui - The olfactory epithelium (OE) maintains lifelong neurogenesis and shows strong regenerative capacity through the coordinated functions of horizontal basal cells (HBCs) and globose basal cells (GBCs). These progenitors are regulated by key transcriptional factors such as Sox2, p63, Pax6, Ascl1, Neurog1 and NeuroD1, as well as signaling pathways including Wnt/β-catenin, Notch, YAP and inflammation-related regulators, which together control lineage specification and injury-induced plasticity. A set of genes such as Lgr5, Tmem59, Notch1, and Chil4 play critical roles in OE homeostasis and regeneration, depending on a broader and highly dynamic network. Recent progress in single-cell transcriptomics, spatial transcriptomics and organoid models has revealed previously unrecognized cell states, differentiation routes and intercellular communications. This review summarizes the molecular and cellular mechanisms that support OE regeneration and highlights emerging technologies that advance understanding the process of olfactory epithelium regeneration and guiding future approaches for restoring olfactory function. - Source: PubMed
Publication date: 2026/06/02
Qi JiamingYu Yiqun - 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