NEUROD4 antibody - middle region (ARP32415_P050)
- Known as:
- NEUROD4 (anti-) - middle region (ARP32415_P050)
- Catalog number:
- arp32415_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- NEUROD4 antibody - middle region (ARP32415_P050)
Related genes to: NEUROD4 antibody - middle region (ARP32415_P050)
- Gene:
- NEUROD4 NIH gene
- Name:
- neuronal differentiation 4
- Previous symbol:
- -
- Synonyms:
- Atoh3, ATH-3, MATH-3, bHLHa4
- Chromosome:
- 12q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-11-28
- Date modifiied:
- 2019-04-16
Related products to: NEUROD4 antibody - middle region (ARP32415_P050)
Related articles to: NEUROD4 antibody - middle region (ARP32415_P050)
- In electroreceptive jawed fishes and amphibians, individual lateral line placodes form lines of neuromasts on the head containing mechanosensory hair cells, flanked by fields of ampullary organs containing electroreceptors-modified hair cells that respond to weak electric fields. Extensively shared gene expression between neuromasts and ampullary organs suggests that conserved molecular mechanisms are involved in their development, but a few transcription factor genes are restricted either to the developing electrosensory or mechanosensory lateral line. Here, we used CRISPR/Cas9-mediated mutagenesis in G0-injected sterlet embryos (, a sturgeon) to test the function of three such genes. We found that the 'hair cell' transcription factor gene is required for both hair cell and electroreceptor differentiation in sterlet, and for and expression in both neuromasts and ampullary organs. These data support the conservation of developmental mechanisms between hair cells and electroreceptors. Targeting ampullary organ-restricted did not yield any phenotype, potentially owing to redundancy with other genes that we found to be expressed in sterlet ampullary organs. After targeting mechanosensory-restricted , ampullary organs formed within neuromast lines, suggesting that FoxG1 normally represses their development, whether directly or indirectly. We speculate that electrosensory organs may be the 'default' developmental fate of lateral line primordia in electroreceptive vertebrates. - Source: PubMed
Publication date: 2025/06/25
Minařík MartinCampbell Alexander SFraněk RomanVazačová MichaelaHavelka MilošGela DavidPšenička MartinBaker Clare V H - Spinal cord injury (SCI) is one of the devastating neurological disorders that leads to a loss of motor and sensory functions. Long non-coding RNA small nucleolar RNA host gene 6 (lncRNA SNHG6) plays a crucial role in inflammatory regulation across various diseases. This study investigates the role of SNHG6 in SCI development and its underlying regulatory mechanisms. Two experimental models were established: an in vitro model using LPS-challenged (100 ng/mL) mouse microglia BV2 cells and an in vivo model employing controlled spinal cord impact in mice. SNHG6, miR-182-5p, and NEUROD4 expression levels were quantified through RT-qPCR and Western blot. Functional and histological assessments were performed using the Basso mouse scale (BMS) and Nissl staining, respectively. Putative binding sites between SNHG6 and miR-182-5p, as well as between miR-182-5p and NEUROD4, were predicted using the ENCORI/starBase platform. These molecular interactions were validated through dual-luciferase reporter assays and RNA pull-down experiments, with further confirmation by qRT-PCR and Western blot analyses. Both LPS-stimulated BV2 cells and spinal cord tissues from SCI mice exhibited elevated SNHG6 expression. Downregulation of SNHG6 enhanced LPS-induced polarization of BV2 cells from M1-type to M2-type, significantly modulated the expression of pro-inflammatory factors (TNF-α, IL-1β, and IL-6) and anti-inflammatory factors (TGF-β, IL-10, and IL-13), and reduced injury severity in SCI mice. Our mechanistic studies revealed that SNHG6 functions as a molecular sponge for miR-182-5p to regulate NEUROD4 expression. This study demonstrates that SNHG6 knockdown promotes microglial M2-type polarization and alleviates inflammatory responses through modulation of the miR-182-5p/NEUROD4 axis, suggesting SNHG6 as a potential therapeutic target for SCI treatment. - Source: PubMed
Publication date: 2025/01/20
Feng LuqianLi Gang - Parkinson's disease (PD) is a complex neurodegenerative disease with unclear pathogenesis. Some recent studies have shown that there is a close relationship between PD and ferroptosis. We aimed to identify the ferroptosis-related genes (FRGs) and construct competing endogenous RNA (ceRNA) networks to further assess the pathogenesis of PD. - Source: PubMed
Publication date: 2024/12/31
Li TaoleGuo Jifeng - - Source: PubMed
Publication date: 2024/12/10
Le Ciclé CharlesPacini VincentRama NicolasTauszig-Delamasure ServaneAiraud ÉloïsePetit Florencede Beco SimonCohen-Tannoudji JoëlleL'Hôte David - Despite strong evidence demonstrating that normal lens development requires regulation governed by microRNAs (miRNAs), the functional role of specific miRNAs in mammalian lens development remains largely unexplored. - Source: PubMed
Upreti AnilHoang Thanh VLi MinghuaTangeman Jared ADierker David SWagner Brad DTsonis Panagiotis ALiang ChunLachke Salil ARobinson Michael L