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Rabbit Anti-CDH23 Recombinant Antibody (EG590) (CBMAB-EN712-LY)

The product is antibody recognizes CDH23. The antibody EG590 immunoassay techniques such as: IF: 1:100~1:500 ELISA: 1:10000.
See all CDH23 antibodies

Summary

Host Animal
Rabbit
Specificity
Human, Mouse, Rat
Clone
EG590
Antibody Isotype
IgG
Application
IF: 1:100~1:500 ELISA: 1:10000

Basic Information

Immunogen
The antibody was produced against synthesized peptide derived from internal of human CDH23.
Specificity
Human, Mouse, Rat
Antibody Isotype
IgG
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
Cadherin Related 23
Introduction
CDH23 (Cadherin Related 23) is a Protein Coding gene. Diseases associated with CDH23 include Deafness, Autosomal Recessive 12 and Usher Syndrome, Type Id. Among its related pathways are ERK Signaling and S-1P Stimulated Signaling. Gene Ontology (GO) annotations related to this gene include calcium ion binding. An important paralog of this gene is FAT3.
Entrez Gene ID
Human64072
Mouse22295
Rat114102
UniProt ID
HumanQ9H251
MouseQ99PF4
RatP58365
Alternative Names
Cadherin Related 23; Cadherin-Related Family Member 23; Cadherin-Like 23; Otocadherin; Cadherin-23; KIAA1774;
Function
Cadherins are calcium-dependent cell adhesion proteins. They preferentially interact with themselves in a homophilic manner in connecting cells. CDH23 is required for establishing and/or maintaining the proper organization of the stereocilia bundle of hair cells in the cochlea and the vestibule during late embryonic/early postnatal development. It is part of the functional network formed by USH1C, USH1G, CDH23 and MYO7A that mediates mechanotransduction in cochlear hair cells. Required for normal hearing.
Biological Process
Calcium-dependent cell-cell adhesion via plasma membrane cell adhesion molecules Source: UniProtKB
Calcium ion transport Source: DFLAT
Cell-cell adhesion via plasma-membrane adhesion molecules Source: GO_Central
Equilibrioception Source: HGNC-UCL
Homophilic cell adhesion via plasma membrane adhesion molecules Source: InterPro
Inner ear receptor cell stereocilium organization Source: InterPro
Locomotory behavior Source: InterPro
Photoreceptor cell maintenance Source: HGNC-UCL
Regulation of cytosolic calcium ion concentration Source: DFLAT
Response to stimulus Source: UniProtKB-KW
Sensory perception of light stimulus Source: HGNC-UCL
Sensory perception of sound Source: HGNC-UCL
Visual perception Source: UniProtKB-KW
Cellular Location
Cell membrane
Involvement in disease
Usher syndrome 1D (USH1D): USH is a genetically heterogeneous condition characterized by the association of retinitis pigmentosa with sensorineural deafness. Age at onset and differences in auditory and vestibular function distinguish Usher syndrome type 1 (USH1), Usher syndrome type 2 (USH2) and Usher syndrome type 3 (USH3). USH1 is characterized by profound congenital sensorineural deafness, absent vestibular function and prepubertal onset of progressive retinitis pigmentosa leading to blindness.
Usher syndrome 1D/F (USH1DF): USH1DF patients are heterozygous for mutations in CDH23 and PCDH15, indicating a digenic inheritance pattern.
Deafness, autosomal recessive, 12 (DFNB12): A form of non-syndromic sensorineural hearing loss. Sensorineural deafness results from damage to the neural receptors of the inner ear, the nerve pathways to the brain, or the area of the brain that receives sound information.
Pituitary adenoma 5, multiple types (PITA5): A form of pituitary adenoma, a neoplasm of the pituitary gland and one of the most common neuroendocrine tumors. Pituitary adenomas are clinically classified as functional and non-functional tumors, and manifest with a variety of features, including local invasion of surrounding structures and excessive hormone secretion. Functional pituitary adenomas are further classified by the type of hormone they secrete: growth hormone (GH)-secreting, prolactin (PRL)-secreting, adrenocorticotropin (ACTH)-secreting, thyroid-stimulating hormone (TSH)-secreting, and plurihormonal (GH and TSH) tumors. Familial and sporadic forms have been reported. The transmission pattern of familial PITA5 is consistent with autosomal dominant inheritance with reduced penetrance.
Topology
Extracellular: 24-3064
Helical: 3065-3085
Cytoplasmic: 3086-3354

Koohiyan, M., Hashemzadeh-Chaleshtori, M., Salehi, M., Abtahi, H., Noori-Daloii, M. R., & Tabatabaiefar, M. A. (2020). A novel cadherin 23 variant for hereditary hearing loss reveals additional support for a DFNB12 nonsyndromic phenotype of CDH23. Audiology and Neurotology, 25(5), 258-262.

Yu, W., Wang, X., Wang, Y., Jiang, Y., Zhang, W., Shi, H., & Li, Y. (2020). A novel highly frequent single‑nucleotide polymorphism site of cadherin 23 in clear cell renal cell carcinoma with sarcomatoid differentiation based on whole exome sequencing. Oncology Reports, 44(2), 735-746.

Hashemzadeh-Chaleshtorib, M. K. M., & Tabatabaiefara, M. A. (2020). A Novel Cadherin 23 Variant for Hereditary Hearing Loss Reveals Additional Support for a DFNB12 Nonsyndromic Phenotype of CDH23.

Zheng, C., Ren, X., Xing, D., Bu, S., Wen, D., He, Y., ... & Li, X. (2020). A novel missense mutation locus of cadherin 23 and the interaction of cadherin 23 and protocadherin 15 in a patient with usher syndrome. Ophthalmic Genetics, 41(5), 501-504.

Sannigrahi, M. K., Srinivas, C. S., Deokate, N., & Rakshit, S. (2019). The strong propensity of Cadherin‐23 for aggregation inhibits cell migration. Molecular oncology, 13(5), 1092-1109.

Xu, T., Zhu, W., Wang, P., Li, H., & Yu, S. (2019). Identification of novel cadherin 23 variants in a Chinese family with hearing loss. Molecular medicine reports, 20(3), 2609-2616.

Jaiganesh, A., De-la-Torre, P., Patel, A. A., Termine, D. J., Velez-Cortes, F., Chen, C., & Sotomayor, M. (2018). Zooming in on cadherin-23: Structural diversity and potential mechanisms of inherited deafness. Structure, 26(9), 1210-1225.

Srisailapathy, C. S., & Mohanram, R. K. (2018). The tip link protein Cadherin-23: From hearing loss to cancer. Pharmacological research, 130, 25-35.

Sannigrahi, M. K., Srinivas, S., & Rakshit, S. (2018). The prospects of cadherin-23 as a mediator of homophilic cell-cell adhesion. Biochemical and Biophysical Roles of Cell Surface Molecules, 99-105.

Zhang, Q., Peng, C., Song, J., Zhang, Y., Chen, J., Song, Z., ... & Zhao, Y. (2017). Germline mutations in CDH23, encoding cadherin-related 23, are associated with both familial and sporadic pituitary adenomas. The American Journal of Human Genetics, 100(5), 817-823.

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For research use only. Not intended for any clinical use.

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