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CDH23 is a member of the cadherin superfamily, whose genes encode calcium dependent cell-cell adhesion glycoproteins. Additionally we are shipping CDH23 Antibodies (51) and CDH23 Kits (7) and many more products for this protein.
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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.
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 (show USH1C Proteins) form a ternary complex and interact with phospholipids.
Mice homozygous for Cdh23 gene mutations exhibit progressive hearing loss.
Four (3.1 %) of 128 children carried two CDH23 mutant alleles, and SLC26A4 (show SLC26A4 Proteins) and GJB2 (show GJB2 Proteins) 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
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 (show USH1C Proteins) 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.
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