POU3F4 antibody - C-terminal region (P100907_T100)
- Known as:
- POU3F4 (anti-) - C-terminal region (P100907_T100)
- Catalog number:
- p100907_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- POU3F4 antibody - C-terminal region (P100907_T100)
Related genes to: POU3F4 antibody - C-terminal region (P100907_T100)
- Gene:
- POU3F4 NIH gene
- Name:
- POU class 3 homeobox 4
- Previous symbol:
- DFN3
- Synonyms:
- BRN4, OTF9, DFNX2
- Chromosome:
- Xq21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-09-30
- Date modifiied:
- 2018-03-06
Related products to: POU3F4 antibody - C-terminal region (P100907_T100)
Related articles to: POU3F4 antibody - C-terminal region (P100907_T100)
- Melanocytes are important components of the inner-ear cellular architecture. However, limited morphological research hinders our understanding of inner-ear function. Here, we characterize the morphology of inner-ear melanocytes and cells often misidentified as melanocytes. Immunofluorescence, smart-seq, transmission/field emission scanning electron microscopy, and immunoelectron microscopy are used. Cells previously referred to as "perivascular macrophage-like melanocytes" are not observed in the stria vascularis and are actually macrophages; along with melanocytes, they constitute intermediate cells. Cells with a "black ball" appearance in the vestibule are identified as macrophages. We examine variation in melanocytes or macrophages with age, strain, and cisplatin injury. Kir4.1 expression and the greater noise resistance observed in pigmented mice suggest melanocyte functions. Based on melanin distribution in Pou3f4 mice, we hypothesize that melanocytes migrate from the modiolus along Reissner's membrane area to the stria vascularis, following a base-to-apex gradient. These findings provide novel ultrastructural and immunological insights into inner-ear function. - Source: PubMed
Publication date: 2026/01/26
Cai JingXu LeiSong YongdongZhang AizhenLi ZhengKong LigangXu KaifanJin YuWang SiyueLu JunzeXiao YunZhang DaogongLi BoqinWang Haibo - X-linked deafness 2 (DFNX2) is a rare hereditary hearing loss characterized by progressive conductive and sensorineural hearing loss and a pathognomonic temporal bone deformity. DFNX2 is caused by mutations in the coding sequence or deletions upstream of . Only 12 upstream deletions of associated with DFNX2 have been reported, and the precise mechanisms underlying its pathogenesis remain fully elucidated. - Source: PubMed
Publication date: 2025/10/16
Yang YantingHuang ShengwenLiu YaoMu DanBai TingJing XiaoshaXing LinglingLiu Hongqian - Many children with neurodevelopmental disorders (NDD) show complex, multidimensional impairments meeting criteria for multiple NDD, yet remain "diagnostically homeless" as DSM-5 lacks a Multidimensional Impairment (MDI) category. We investigated the prevalence of genetic abnormalities in such complex NDD cases. - Source: PubMed
Publication date: 2025/10/02
Hanin CyrilTorres PalomaMillet IsabelleMatos JoanaCravero CoraGiannitelli MariannaPellen Anne-SophiePellerin HuguesGrossard CharlineZammouri IngridDe Foucaud AstridLaurent-Levinson ClaudineCohen David - Prelingual sensorineural hearing loss (SNHL) represents about 80% of genetic SNHL, with at least 90 causative genes identified. In order to identify the genetic diagnosis of prelingual SNHL, we performed a prospective study by systematic history-taking and phenotyping, followed by whole-exome sequencing (WES) with target gene analysis in 100 Thai patients. We found an overall diagnostic yield of 46%, 58.3% for familial cases, and 39.0% for sporadic cases. These included 41 cases with nonsyndromic SNHL(nsSNHL) and 5 cases with syndromic SNHL (sSNHL). We identified 41 P/LP and 4 VUS variants of 15 genes. Of those sSNHL, the causative genes were PAX3, SOX10, MITF (Waardenburg and Teitz syndromes), and SLC26A4 (Pendred syndrome). The genetic defects identified among those with nsSNHL were GJB2 and SLC26A4 as the most prevalent causes, followed by MYO15A, MYO7A, POU3F4, OTOF, PCDH15, GSDME, PTEN, ACTG1, TMPRSS3, MITF, and MPZL2. The inheritance of these nsSNHL genes involved X-linked recessive (n = 3), autosomal dominant (n = 3), and autosomal recessive in the remainder (n = 36). Patients with positive mutations underwent surveillance for associated symptoms like goiter and retinitis pigmentosa. In conclusion, most prelingual SNHL was nsSNHL with autosomal recessive inheritance. Identifying the causative gene benefits patients for specific management and genetic counseling. - Source: PubMed
Publication date: 2025/09/25
Damrongchietanon TasyakornWattanasirichaigoon DuangrurdeeKhongkraparn ArthapornNoojarern SaisudaTiravanitchakul RattinanKasemkosin NittayaKiatthanabumrung SivapornTim-Aroon ThipwimolWongkittichote Parith - To investigate the molecular findings and long-term outcomes of cochlear implantation (CI) in a relatively large cohort of patients with incomplete partition type-III malformation (IP-III), and to analyze the correlation between genotype and CI outcomes. - Source: PubMed
Publication date: 2025/06/03
Chao XiuhuaLuo JianfenXiao YunWang RuijieJi ShuhuaHu FangxiaFan ZhaominWang HaiboXu Lei