POU4F3 antibody - middle region (ARP33065_T100)
- Known as:
- POU4F3 (anti-) - middle region (ARP33065_T100)
- Catalog number:
- arp33065_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- POU4F3 antibody - middle region (ARP33065_T100)
Related genes to: POU4F3 antibody - middle region (ARP33065_T100)
- Gene:
- POU4F3 NIH gene
- Name:
- POU class 4 homeobox 3
- Previous symbol:
- DFNA15, DFNA52, DFNA42
- Synonyms:
- BRN3C
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-07
- Date modifiied:
- 2019-04-23
Related products to: POU4F3 antibody - middle region (ARP33065_T100)
Related articles to: POU4F3 antibody - middle region (ARP33065_T100)
- Adult human inner ear hair cells have extremely limited regenerative ability, and the inaccessibility of human inner ear tissue makes studying regeneration challenging. In this study, we examined whether 5-azacytidine (5-aza) could induce hair cell-like differentiation using our previously established human utricular cell (HUC) line. Our results showed that treatment with 40-80 μM 5-aza was non-toxic, as confirmed by cell counting and calcein/propidium iodide assays. BrdU incorporation analysis showed that fewer treated HUCs entered the S-phase, indicating reduced cell proliferation following 5-aza treatment. Reverse transcription PCR revealed that 5-aza induced the expression of hair cell genes (Myo7a, Pou4f3, Atoh1, and Myo6), which were absent in untreated cells. Immunofluorescence confirmed the expression of hair cell proteins in 5-aza-treated cells, including Myosin VIIa, Pou4f3, Atoh1, Myosin VI, and Calretinin. Additionally, FM1-43 uptake assays indicated the emergence of functional mechanotransduction-like channels in 5-aza-treated HUCs. Together, these results demonstrate that 5-aza reduces proliferation and promotes differentiation of HUCs toward a hair cell-like phenotype. This finding provides new insight into the molecular mechanisms regulating human sensory hair cell differentiation in vitro and highlights the potential of HUCs as a model for studying human inner ear hair cell regeneration. - Source: PubMed
Publication date: 2026/02/25
Deng MengHu Zhengqing - Approximately 200 genes have been identified as causative in hereditary hearing loss. Genetic testing is increasingly important, not only for accurate diagnosis but also for predicting audiometric profiles, prognoses, and potential syndromic features. Hereditary hearing loss can be syndromic or nonsyndromic, with nonsyndromic forms further classified by inheritance: autosomal-dominant or autosomal-recessive. In autosomal-dominant cases, three pathological mechanisms-haploinsufficiency, dominant-negative effects, and gain of function-are often implicated. Moreover, specific genes correlate with distinct audiometric patterns: WFS1 variants typically cause low-frequency hearing loss, whereas KCNQ4 and POU4F3 variants are linked to high-frequency loss. To investigate the underlying mechanisms of these frequency-dependent patterns, gene expression across cochlear turns was compared in mice, but interpretations of the results were limited because of inherent structural differences between rodent and primate cochleae. Therefore, the common marmoset (Callithrix jacchus), which offers closer anatomical and functional similarity to human cochleae, was utilized herein as an improved model. Using RNA sequencing (RNA-seq) across cochlear turns of common marmosets, the present study aimed to uncover gene expression and alternative splicing patterns that may explain tonotopic manifestations in hereditary hearing loss, including those caused by WFS1 variants, the present study being one such using common marmoset cochlear RNA-seq data, and these findings are highly valuable for genetic diagnosis and the development of gene therapies. - Source: PubMed
Publication date: 2026/02/07
Yokota ShuYoshimura HidekaneNishio Shin-YaSasaki ErikaMukasa KeisukeUsami Shin-IchiTakumi Yutaka - Over 15% of cancers worldwide are caused by viruses. Merkel cell polyomavirus (MCPyV) is the most recently discovered human oncovirus and is the only polyomavirus that drives malignant tumors in humans. Here, we show that MCPyV+ Merkel cell carcinoma is defined by neuroendocrine-lineage core regulatory (CR) transcription factors (TFs) (ATOH1, INSM1, ISL1, LHX3, POU4F3, and SOX2) that were essential for tumor survival and that co-bound chromatin with the viral small T antigen at super enhancers. Moreover, MCPyV integration sites were enriched at these neuroendocrine super enhancers. We further discovered that the MCPyV noncoding control region contained a homeodomain binding motif absent in other polyomaviruses that bound ISL1 and LHX3 and depended on them for T antigen expression. To therapeutically target the CR factors, we used histone deacetylase (HDAC) inhibitors to collapse the chromatin architecture and induce topological blurring of superenhancer loops, abrogating core TF expression and halting tumor growth. To our knowledge, our study presents the first example of oncogenic cross-regulation between viral and human epigenomic circuitry to generate interlocking and essential transcriptional feedback circuits that explain why MCPyV causes neuroendocrine cancer and represent a tumor dependency that can be targeted therapeutically. - Source: PubMed
Publication date: 2025/12/15
Miao LinglingMilewski DavidCoxon AmyGelb TaraGarman Khalid APorch JadonKhanna ArushiCollado LorenHill Natasha TDaily KennethVilasi SerenaReed DanielleAlexander TiffanyStarrett Gabriel JChakraborty MaharshiSong YoungChoi RachelGangalapudi VineelaSeaman JosiahMorton AndrewBusam Klaus JVakoc Christopher RUrban Daniel JShen MinHall Matthew DSallari RichardKhan JavedGryder Berkley EBrownell Isaac - Sensory neurotoxicity involves damage to the sensory nerves, often resulting from exposure to chemicals, medications, toxins, infections, or neurological disorders. Benzalkonium chloride (BKC) is a widely used quaternary ammonium compound with antiseptic properties, commonly present in pharmaceuticals, household products, and cosmetics. While the potential neurotoxicity of BKC has been previously explored in ocular and nasal epithelia, its impact on other sensory systems and the underlying mechanisms remain largely unclear. In this study, we used zebrafish (Danio rerio) embryos to assess the developmental neurotoxicity of BKC. Embryonic exposure to 0.72, 1.28, and 2.24 mg/L BKC led to dose-dependent impairments in mechanosensory hair cells, reduced startle responses, and heightened nociceptive sensitivity upon noxious stimulation. BKC exposure induced pronounced oxidative stress, evidenced by increased reactive oxygen species levels, reduced antioxidant enzyme activity, and altered expression of redox-regulating genes. Moreover, BKC significantly upregulated inflammatory and pain-associated genes, including tnfa, il1b, cox2, bdnf, and trpa1b. Expression profiling of hair cell differentiation markers revealed increased pou4f3 and decreased tmc2a/tmc2b, suggesting that BKC disrupts both terminal differentiation and mechanotransduction processes in sensory hair cells. Collectively, these findings uncover a novel mechanistic link between oxidative stress, impaired hair-cell maturation, and sensory dysfunction, offering new insights into the mechanisms underlying BKC-induced sensory neurotoxicity. This study emphasizes the ecological and toxicological relevance of quaternary ammonium compounds in aquatic environments. - Source: PubMed
Publication date: 2025/12/12
Kim YeonhwaCho YujiJeon Eun JungJeong Sang HoonPark Eun-KeePark Hae-ChulLee Ju-HanKim Suhyun - Inner ear hair cells are mechanoreceptors critical for hearing and balance. Damage to vestibular hair cells causes balance impairment, yet it is unclear whether hair cell loss correlates with vestibular dysfunction. In this study, we ablated hair cells in mice with diphtheria toxin (DT), and found a dose-dependent decrease in hair cell survival in both the macula and crista ampullaris, including loss of type I and II hair cells in the striolar/central and extrastriolar/peripheral regions. Responses to linear acceleration, measured by the translational vestibulo-ocular reflex (tVOR) and vestibular sensory evoked potential (VsEP), were intact with 25% or more hair cell survival in the macula, and diminished only when hair cell survival decreased further. By contrast, rotational vestibulo-ocular reflex (rVOR) responses were significantly reduced with ∼31% hair cell survival in the cristae. Further, single-unit recordings of vestibular afferents from cristae and maculae showed more irregular and reduced firing rates, but only those corresponding to cristae displayed reduced sensitivity to head rotation. Limited hair cell regeneration was observed in the extrastriolar/peripheral regions of both maculae and cristae 6 months post ablation, although no significant recovery of the VORs was observed. Thus, the adult mouse vestibular end organs display different degrees of redundancy, demonstrating robust responses to head rotation and linear acceleration despite loss of most hair cells. - Source: PubMed
Publication date: 2025/12/02
Wang TianHosseini Davood KMahhoudi AhmadSayyid Zahra NHe JunSit CarolineIriarte Oporto Zelma GZhu HongZhou WuCheng Alan G