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anti-Human CLDN14 Antibodies:
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Human Polyclonal CLDN14 Primary Antibody for WB - ABIN1881208
Thorleifsson, Holm, Edvardsson, Walters, Styrkarsdottir, Gudbjartsson, Sulem, Halldorsson, de Vegt, dAncona, den Heijer, Franzson, Christiansen, Alexandersen, Rafnar, Kristjansson: Sequence variants in the CLDN14 gene associate with kidney stones and bone mineral density. in Nature genetics 2009
Show all 3 Pubmed References
Human Polyclonal CLDN14 Primary Antibody for IHC (p), IHC - ABIN249595
Sato, Hiraoka, Suzuki, Bai, Kurotani, Yokoyama, Okumura, Cismowski, Lanier, Ishikawa: Identification of transcription factor E3 (TFE3) as a receptor-independent activator of Gα16: gene regulation by nuclear Gα subunit and its activator. in The Journal of biological chemistry 2011
Show all 2 Pubmed References
Human Polyclonal CLDN14 Primary Antibody for ELISA, WB - ABIN546891
Wilcox, Burton, Naz, Riazuddin, Smith, Ploplis, Belyantseva, Ben-Yosef, Liburd, Morell, Kachar, Wu, Griffith, Riazuddin, Friedman: Mutations in the gene encoding tight junction claudin-14 cause autosomal recessive deafness DFNB29. in Cell 2001
This study suggested considerable genetic heterogeneity in the causation of hearing loss in Dhadkai. Recessive mutations were observed in at least three genes causing hearing loss: OTOF (p.R708X), SLC26A4 (p.Y556X) and CLDN14 (p.V85D). Mutation p.R708X appeared to be the major cause of hearing impairment in Dhadkai.
CLDN14 might not be a major causative gene for NSHL in Chinese populations, which would contribute to fully understanding the genetic cause of NSHL in the East Asian populations
Our data suggest that children with the INSM1 binding site within the CLDN14 risk haplotype have a higher likelihood of hypercalciuria and kidney stones. Enhanced CLDN14 expression may play a role in the pathophysiology of their hypercalciuria.
All hearing impaired individuals, including the proband, are homozygous for a pathogenic variant of CLDN14, but this only explains the deafness.
Extensive clinical recruitment and targeted screening suggest that CLDN14 p.(Ala163Val) represents a major founder variant for prelingual sensorineural hearing loss in the Newfoundland population.
CLDN14 is a novel direct target of EZH2-mediated H3K27ME3 and plays role in EZH2-H3K27ME3-mediated hepatocellular carcinoma aggressiveness.
The rs170183 was correlated with a decline in claudin 14 expression in both lymphoblastoid cell lines and T cells.
Rs1801725 (Ala986-Ser), rs1042636 (Arg990Gly) of CaSR gene and rs219778, rs219780 (Thr229Thr) of CLDN14 gene were significantly associated with kidney stone disease in patients from the Eastern part of India.
Claudin 14 expression was up-regulated in gastric cancer.
Data suggest a possible role for Claudin14 in urinary calcium excretion.
CLDN14 mutations can contribute to the aetiology of childhood/congenital deafness in Moroccan patients.
Human Cldn-8 and -14 were shown to convey Clostridium perfringens enterotoxin-mediated cytotoxicity at pathophysiologically relevant concentrations of this toxin, although ~2-to-10-fold less efficiently than Cldn-4.
OPRM1 genetic polymorphisms are associated with the plasma concentration of cotinine in a Taiwanese MMT cohort. Carriers with the major allele of SNP rs1799971 had a higher plasma cotinine concentration.
The hearing loss due to novel CLDN14 mutations is prelingual, severe-to-profound with greater loss in the high frequencies.
The CLDN14 promoter is activated by Trichostatin A (TSA) treatment according to promoter reporter assays in HEK 293 cells.
Individuals with mutations of CLDN14 may have different degrees of hearing loss and the loss is greater at higher frequencies.
The palmitoylation of claudin-14 is required for efficient localization into tight junctions but not stability or strand assembly.
The ability of CLDN14 to be recruited to these junctions is crucial for the hearing process.
Common, synonymous variants in the CLDN14 gene that associate with kidney stones, were discovered.
These findings suggest that (1) the changes in endolymphatic ion concentrations might not be involved in hair cells degeneration in Cldn14(-/-), (2) [Ca]e might be regulated by endocochlear potential in both Wt and Cldn14(-/-).
High Cldn14 is associated with hypoparathyroidism.
claudin-14-targeting miR-9 and miR-374, rather than promoter of the claudin-14 gene itself, regulated through histone deacetylation
describe a CaSR-NFATc1-microRNA-claudin-14 signaling pathway in the kidney that underlies paracellular Ca(++) reabsorption through the tight junction
Stromal Claudin14-heterozygosity, but not deletion, increases tumor blood leakage without affecting tumor growth.
Activation of the Ca(2+)-sensing receptor in the thick ascending limb increases Cldn14 expression, which in turn blocks the paracellular reabsorption of Ca(2+).
MiR-9 and miR-374 transcript levels are regulated by extracellular Ca(++) in a reciprocal manner as claudin-14.
To explore the role of claudin 14 in the inner ear and in other tissues we created a mouse model by a targeted deletion of Cldn14.
We generated claudin 11/claudin 14 double-deficient mice, which exhibit deafness, neurological deficits, and male sterility. Kidney function and ion balance are not significantly affected.
Tight junctions represent one mode of cell-to-cell adhesion in epithelial or endothelial cell sheets, forming continuous seals around cells and serving as a physical barrier to prevent solutes and water from passing freely through the paracellular space. These junctions are comprised of sets of continuous networking strands in the outwardly facing cytoplasmic leaflet, with complementary grooves in the inwardly facing extracytoplasmic leaflet. The protein encoded by this gene, a member of the claudin family, is an integral membrane protein and a component of tight junction strands. The encoded protein also binds specifically to the WW domain of Yes-associated protein. Defects in this gene are the cause of an autosomal recessive form of nonsyndromic sensorineural deafness. It is also reported that four synonymous variants in this gene are associated with kidney stones and reduced bone mineral density. Several transcript variants encoding the same protein have been found for this gene.