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anti-Mouse (Murine) CDH23 Antikörper:
anti-Human CDH23 Antikörper:
anti-Rat (Rattus) CDH23 Antikörper:
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Human Polyclonal CDH23 Primary Antibody für ELISA, WB - ABIN449707
Roux, Faugère, Le Guédard, Pallares-Ruiz, Vielle, Chambert, Marlin, Hamel, Gilbert, Malcolm, Claustres: Survey of the frequency of USH1 gene mutations in a cohort of Usher patients shows the importance of cadherin 23 and protocadherin 15 genes and establishes a detection rate of above 90%. in Journal of medical genetics 2006
Human Polyclonal CDH23 Primary Antibody für ELISA, WB - ABIN566227
Apostolopoulou, Ligon: Cadherin-23 mediates heterotypic cell-cell adhesion between breast cancer epithelial cells and fibroblasts. in PLoS ONE 2012
Data indicate that cadherin 23 (CDH23) EC1+2 from the erl mice showed less Ca(2+)-dependent proteolysis protection comparing with that of the wild type control.
The results illustrate the large effects that the mouse strain background and congenic regions have on the hearing loss associated with Cdh23 alleles.
Many GABAergic interneurons, from their generation in the medial ganglionic eminence up to their settlement in the auditory cortex, express two cadherin-related (cdhr) proteins, cdhr23 and cdhr15, that form the hair bundle tip links gating the mechanoelectrical transduction channels.
data suggest that CDH23-C is a CAMSAP3/Marshalin-binding protein that can modify MT networks indirectly through its interaction with CAMSAP3/Marshalin.
interactions of wild type (WT) and mutant variants of N-terminal fragments (EC1+2) of cadherin-23 and protocadherin-15, two proteins essential for inner-ear mechanotransduction, are reported.
It affects inner ear structures and results in age-related hearing loss.
These results clearly show that the development of early-onset progressive hearing loss (ePHL) requires at least two mutant alleles of the Ush1g and Cdh23 genes. Our results also suggest that because the SANS and CDH23 proteins form a complex in the stereocilia, the interaction between these proteins may play key roles in the maintenance of stereocilia and the prevention of ePHL.
Our results showed that systemic treatment with TUDCA significantly alleviated hearing loss and suppressed hair cell death in erl(Cdh23) mice. Additionally.
This study further resolves the interaction between Atp2b2 and Cdh23 in a gene dosage and frequency-dependent manner, and finds that low auditory frequencies are significantly affected by the interaction.
It plays an important role in the maintenence of tip links of stereocilia during the aging process.
crystallography, molecular dynamics simulations and binding experiments to characterize the protocadherin 15-cadherin 23 bond
A point mutation in the Cdh23 gene (208T>C) of C57BL/6J mice results in hearing loss around 1 month after birth.
the Cdh23(nmf308/nmf308) mice with progressive hair cell loss had specific morphological changes and suffered a base to apex gradient and age-related hearing loss (AHL), and that mutations in cdh23 were linked to AHL
A novel synaptic Usher complex comprised of clarin-1 and specific isoforms of CDH23, PCDH15 and VLGR1, was identified.
Although Cdh23(ahl) homozygosity is necessary, it is not by itself sufficient to account for the accelerated hearing loss of C57BL/6J mice.
ENU-induced mutation of Cdh23 causes congenital hearing loss, but no vestibular dysfunction, in mice
results therefore provide genetic evidence consistent with PCDH15 and CDH23 being part of the tip-link complex and necessary for normal mechanotransduction
Cadherin-23, myosin VIIa and harmonin form a ternary complex and interact with phospholipids.
Mice homozygous for Cdh23 gene mutations exhibit progressive hearing loss.
Functional interaction of cadherin-23 with protocadherin-15 is required for the development of sensory transduction in auditory hair cells.
19 variants including 6 pathogenic missense mutations were identified among South Indian assortative mating hearing-impaired individuals
We have identified CDH23 mutations as a genetic risk factor for both familial and sporadic pituitary adenoma.
an important contribution of CDH23 mutations to poslingual Sensorineural Hearing Loss
A new diagnosis of sector retinitis pigmentosa was found to have two novel compound heterozygous mutations in CDH23, including one missense (c.8530C > A; p.Pro2844Thr) and one splice-site (c.5820 + 5G > A) mutation.
Four (3.1 %) of 128 children carried two CDH23 mutant alleles, and SLC26A4 and GJB2 accounted for 18.0 and 17.2 %, respectively and showed profound nonsyndromic sensorineural hearing loss with minimal residual hearing.
The results revealed that CDH23 mutations are highly prevalent in patients with congenital high-frequency sporadic or recessively inherited hearing loss
possible role in the deterioration of kidney function [meta-analysis]
Description of the spectrum of mutations in CDH23 in 374 families with autosomal recessive, non-syndromic hearing loss from India.
The results of this study confirm that CDH23 genetic variant may modify the susceptibility to noise-induced hearing loss development in humans
mutations in the CDH23 gene are one of the most important causes of non-syndromic hearing loss in East Asians.
Hearing loss was found to co-segregate with locus-specific STR markers for CDH23 in 1 Pakistani family.
mutations of the CDH23 gene are an important cause of non-syndromic hearing loss.
Large protein assemblies formed by multivalent interactions between cadherin23 and harmonin suggest a stable anchorage structure at the tip link of stereocilia
Despite that the Ahl allele of Cdh23 had been implicated with ARHI in mice, we found no positive association of the CDH23 tag SNP in intron 7 with ARHI in Han Chinese.
cadherin-23 is up-regulated in breast cancer tissue versus normal tissue and we propose that cadherin-23-mediated heterotypic adhesion between invading tumor cells and stromal fibroblasts may play a role in the metastatic cascade.
One non-syndromic deafness allele (DFNB12) in trans configuration to an Usher syndrome allele (USH1D) of CDH23 preserves vision and balance in deaf individuals, indicating that the DFNB12 allele is phenotypically dominant to an USH1D allele.
Five mutations (three in MYO7A and two in CDH23) were identified in four of five unrelated patients with Usher syndrome type 1.
individuals with the rs1227049 CC genotype, rs3802711 TT genotype and GG genotype in the terminal position of exon 7 of CDH23 might be more susceptible to noise induced hearing loss.
determined the structure of the extracellular cadherin (EC)1-EC2 domains of cadherin 23, which binds to protocadherin 15 to form tip links of mechanosensory hair cells.
This gene is a member of the cadherin superfamily, whose genes encode calcium dependent cell-cell adhesion glycoproteins. The encoded protein is thought to be involved in stereocilia organization and hair bundle formation. The gene is located in a region containing the human deafness loci DFNB12 and USH1D. Usher syndrome 1D and nonsyndromic autosomal recessive deafness DFNB12 are caused by allelic mutations of this cadherin-like gene. Alternative splice variants encoding different isoforms have been described.
age related hearing loss 1
, modifier of deaf waddler
, cadherin-like 23
, cadherin-related family member 23
, cadherin 23 (otocadherin)
, cadherin related 23