Monkey PCDH15 (Protocadherin 15) ELISA Kit
- Known as:
- Monkey PCDH15 (Protocadherin 15) Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- e-el-mk0759
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Elabscience
- Gene target:
- Monkey PCDH15 (Protocadherin 15) ELISA Kit
Related genes to: Monkey PCDH15 (Protocadherin 15) ELISA Kit
- Gene:
- PCDH15 NIH gene
- Name:
- protocadherin related 15
- Previous symbol:
- USH1F, DFNB23
- Synonyms:
- CDHR15
- Chromosome:
- 10q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-02-27
- Date modifiied:
- 2016-06-08
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- Tip links connect the stereocilia of mechanosensory hair cells in the inner ear and transmit force onto mechanotransduction (MET) channels. Tip links consist of protocadherin 15 (PCDH15) and cadherin 23, which assemble into an extracellular filament approximately 150 nm in length. Rare freeze-etched electron microscopy (EM) images have suggested that tip links could be right-handed double helices in vivo, but direct structural evidence has been lacking. Using cryo-EM we determined the structure of a large part of the extracellular PCDH15 domain. Two PCDH15 molecules form a parallel cis dimer stabilized by several dimerization interfaces, including two strand crossovers and two parallel contacts, yielding a right-handed double helix. Functional studies show that mutations in PCDH15 dimerization-domains impair MET. Our results establish the molecular foundation for how PCDH15 forms a right-handed double helix to enable mechanical sensing. - Source: PubMed
Publication date: 2026/06/09
Liang XiaopingPathak RoshanQiu XufengDillard LucasTwomey Edward CMüller Ulrich
- Source: PubMed
- With orthologs for >70% of human genes, zebrafish represent a popular model for investigating development and disease, particularly when murine models are unsuitable. One caveat of zebrafish genetic models is the prevalence of paralogs, where compensation and transcriptional adaptation can complicate our understanding. Usher syndrome type 1 F (USH1F), caused by PCDH15 mutations, exemplifies the need for alternatives models; the primary site of injury, calyceal processes (CP), are uniquely lacking from photoreceptors of nocturnal rodents. Here we demonstrate that contrary to previous reports, zebrafish pcdh15a/b paralogs are not absolutely restricted to ear and eye tissues respectively. Instead, both paralogs are expressed and required in the mechanosensitive hair cells and retinal photoreceptors. Double mutants present the most severe phenotypes: loss of kinocilial and stereocilial links in the ear, and disorganization of CPs, inner/outer segment detachment, and photoreceptor cell death. We also demonstrate that ear and eye-specific phenotypes may be isolated via isoform-specific knockout. These data highlight the strengths of zebrafish to study pathomechanism in vivo. They should also caution researchers from defining paralogs as discrete, absolutely restricted functional units without exceptional evidence. When possible, double mutants may be preferable for studying gene function, and modelling diseases where humans have a single ortholog. - Source: PubMed
Publication date: 2026/05/18
Chrystal Paul WKuzmanova LisaLiu JingpinIzvorean AlexaMajeed IshmaelTjoenardi Jefferson FLin QianTropepe Vincent - Variants of at least twenty-seven human genes are associated with stable or progressive nonsyndromic moderate to severe hearing loss inherited as a recessive condition. We ascertained 54 consanguineous families, predominantly from the Punjab province in Pakistan, with multiple individuals affected by moderate to severe or progressively profound hearing loss. After Sanger sequencing identified 4 families with GJB2 variants or a non-coding pathogenic variant in HGF, exome sequencing was carried out for selected samples from the remaining 50 families. Analyses revealed a total of 24 novel and 33 reported variants in 26 different genes associated with hearing loss. Overall, there were 23 missense variants, 3 in-frame deletions and 1 intronic deletion, while 30 variants likely impacted splicing, introduced premature termination codons or caused frameshifts. Thus, over half of the alleles are predicted to severely impair gene function. Genetic heterogeneity was observed in members of 9 families. Variants of SLC26A4 were key contributors with a frequency of 30%, while those affecting CDH23, MYO15A, GJB2 and OTOF explained 28% of hearing loss. Our findings corroborate the contribution of many well-studied gene variants associated with hearing loss and also implicate LHFPL5 and PCDH15 in the etiology of moderate or progressive hearing loss. - Source: PubMed
Publication date: 2026/05/05
Ramzan MemoonaIdrees HafizaKhan HinaFaridi RabiaMunir ZunairaMuzaffar FarihaShabbir KanwalImtiaz AyeshaNoman MuhammadAhmed AlinaBashir RasheedaKhan Niaz MuhammadMaqsood AzraMujtaba GhulamSalman MidhatBukhari IhtishamMunir Hafiz Muhammad WaqasTariq HumaWaqas MuhammadIqbal Muhammad NWohler ElizabethWitmer P DaneSobreira NaraMorell Robert JSeo Go HunInagaki SayakaFriedman Thomas BNaz Sadaf - Cone-rod dystrophy (CRD) is a macular degeneration disorder characterized by initial cone cell degeneration. Mutations in CDHR1, a photoreceptor-specific cadherin, have been found to be associated with the incidence of CRD. While studying the function of CDHR1, we observed that the localization of the zebrafish homologue, cdhr1a, resembles that of calyceal process (CPs). When co-labeling CPs using pcdh15b, we observed that cdhr1a, in the outer segment (OS), juxtaposes with pcdh15b, found in the CP. Similar localization patterns were detected in human, macaque, xenopus, ducks, gerbil, and mouse. Using immunoprecipitation and K652 cell aggregation assays, we demonstrate that pcdh15b and cdhr1a can interact and thus potentially link the OS and CP. To analyze the consequences of OS-CP interactions in CRD, we established a mutant line (). Homozygous mutants exhibit minor cone OS defects starting at 15 dpf and severe OS disruption and cell loss by 3 months. Shortening of CPs coincided with cone OS defects which were significantly exacerbated when combined with the loss of pcdh15b. Rod OS defects were mild and delayed until 3-6 months. In conclusion, we propose that cdhr1a and pcdh15b function to link cone OSs with CPs and maintain OS integrity. - Source: PubMed
Publication date: 2026/04/17
Patel Meet KPiedade Warlen PereiraFamulski Jakub K