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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Claudin 14

CLDN14, claudin-14, DFNB29
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. [provided by RefSeq, Jun 2010] (from NCBI)
Top mentioned proteins: V1a, CAN, OUT, Occludin, Cx26
Papers on CLDN14
Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis: clinical and molecular characteristics.
Claverie-Martin, Santa Cruz de Tenerife, Spain. In Clin Kidney J, Dec 2015
A recent finding has established that another member of the claudin family, claudin-14, plays a key regulatory role in paracellular cation reabsorption by inhibiting the claudin-16-claudin-19 complex.
Corticomedullary difference in the effects of dietary Ca(2+) on tight junction properties in thick ascending limbs of Henle's loop.
Himmerkus et al., Kiel, Germany. In Pflugers Arch, Nov 2015
Expression, localisation and regulation of claudins 10, 14, 16 and 19 differed along the corticomedullary axis: Towards the cortex, the main site of divalent cation reabsorption in TAL, high-Ca(2+) intake led to a strong upregulation of claudin-14 within TAL TJs while claudin-16 and -19 were unaltered.
Molecular Distribution of Deafness Loci in Various Ethnic Groups of the Punjab, Pakistan.
Rasheed et al., Lahore, Pakistan. In J Coll Physicians Surg Pak, Aug 2015
Three families (SAPun-03, SAPun-10 and SAPun-15) were found linked to DFNB12; two families (SAPun-05 and SAPun-17) were found linked to DFNB8/10, while three families (SAPun-06, SAPun-13 and SAPun-19) were found linked to DFNB29, DFNB36 and DFNB37 respectively.
Epigenetic regulation of microRNAs controlling CLDN14 expression as a mechanism for renal calcium handling.
Hou et al., Kiel, Germany. In J Am Soc Nephrol, Mar 2015
Multiple genetic linkage and association studies identified three tight junction genes from the kidney--claudin-14, -16, and -19--as critical for calcium imbalance diseases.
Claudins and the kidney.
Yu, Kansas City, United States. In J Am Soc Nephrol, 2015
Genetic mutations in claudin-16 and -19 cause familial hypomagnesemic hypercalciuria with nephrocalcinosis, whereas polymorphisms in claudin-14 are associated with kidney stone risk.
The effects of claudin 14 during early Wallerian degeneration after sciatic nerve injury.
Yao et al., Nantong, China. In Neural Regen Res, 2015
Claudin 14 has been shown to promote nerve repair and regeneration in the early stages of Wallerian degeneration (0-4 days) in rats with sciatic nerve injury, but the mechanism underlying this process remains poorly understood.
Role of claudins in renal calcium handling.
Negri, Buenos Aires, Argentina. In Nefrologia, 2014
Recent studies have shown that claudin-14 promoting activity is only located in ATLH.
Polymorphisms in CaSR and CLDN14 Genes Associated with Increased Risk of Kidney Stone Disease in Patients from the Eastern Part of India.
Das et al., Calcutta, India. In Plos One, 2014
This study aimed to evaluate the association between genetic defects in vitamin D receptor (VDR), calcium sensing receptor (CaSR) and claudin 14 (CLDN14) genes and kidney stone disease in patients from eastern India.
Rs219780 SNP of Claudin 14 Gene is not Related to Clinical Expression in Primary Hyperparathyroidism.
Amado et al., In Clin Lab, 2014
BACKGROUND: The CLDN14 gene encodes a protein involved in the regulation of paracellular permeability or ion transport at epithelial tight junctions as in the nephron.
New functional aspects of the extracellular calcium-sensing receptor.
Toka, Boston, United States. In Curr Opin Nephrol Hypertens, 2014
CaSR modulates claudin 14, the gatekeeper of paracellular ion transport in the thick ascending limb that is associated with urinary calcium excretion.
Idiopathic calcium nephrolithiasis: a review of pathogenic mechanisms in the light of genetic studies.
Vezzoli et al., Milano, Italy. In Am J Nephrol, 2013
Polymorphisms of eleven genes have been associated with stones in genome-wide association studies and replicated candidate-gene association studies: VDR, SLC34A1, SLC34A4, CLDN14, and CaSR genes coding for proteins regulating tubular phosphate and calcium reabsorption; CaSR, MGP, OPN, PLAU, and UMOD genes coding for proteins preventing calcium salt precipitation; AQP1 gene coding for a water channel in the proximal tubule.
The role of claudin in hypercalciuric nephrolithiasis.
Hou, Saint Louis, United States. In Curr Urol Rep, 2013
The susceptible genes include NKCC2, ROMK and ClCkb/Barttin that underlie renal salt excretion; claudin-14, -16 and -19 that underlie renal Ca(++) excretion; and CaSR that provides a sensing mechanism for the kidney to regulate salt, water and Ca(++) homeostasis.
Claudins and the kidney.
Yu et al., Saint Louis, United States. In Annu Rev Physiol, 2012
Recent evidence has identified claudin-2 as constituting the cation-reabsorptive pathway in the proximal tubule; claudin-14, -16, and -19 as forming a complex that regulates calcium transport in the thick ascending limb of the loop of Henle; and claudin-4, -7, and -8 as determinants of collecting duct chloride permeability.
Claudin-14 regulates renal Ca⁺⁺ transport in response to CaSR signalling via a novel microRNA pathway.
Hou et al., Saint Louis, United States. In Embo J, 2012
MiR-9 and miR-374 transcript levels are regulated by extracellular Ca(++) in a reciprocal manner as claudin-14.
Novel CLDN14 mutations in Pakistani families with autosomal recessive non-syndromic hearing loss.
Leal et al., Houston, United States. In Am J Med Genet A, 2012
The hearing loss due to novel CLDN14 mutations is prelingual, severe-to-profound with greater loss in the high frequencies.
Mutations in CLDN14 are associated with different hearing thresholds.
Naz et al., Lahore, Pakistan. In J Hum Genet, 2010
Individuals with mutations of CLDN14 may have different degrees of hearing loss and the loss is greater at higher frequencies.
Functional analysis and identification of cis-regulatory elements of human chromosome 21 gene promoters.
Yaspo et al., Berlin, Germany. In Nucleic Acids Res, 2010
The CLDN14 promoter is activated by Trichostatin A (TSA) treatment according to promoter reporter assays in HEK 293 cells.
Sequence variants in the CLDN14 gene associate with kidney stones and bone mineral density.
Stefansson et al., Reykjavík, Iceland. In Nat Genet, 2009
Common, synonymous variants in the CLDN14 gene that associate with kidney stones, were discovered.
Mutations in the gene encoding tight junction claudin-14 cause autosomal recessive deafness DFNB29.
Friedman et al., Rockville, United States. In Cell, 2001
The essential function of one of these claudins in the inner ear was established by identifying mutations in CLDN14 that cause nonsyndromic recessive deafness DFNB29 in two large consanguineous Pakistani families.
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