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Human Polyclonal SLC26A4 Primary Antibody für ELISA, WB - ABIN562168
Garnett, Hickman, Burrows, Hegyi, Tiszlavicz, Cuthbert, Fong, Gray: Novel role for pendrin in orchestrating bicarbonate secretion in cystic fibrosis transmembrane conductance regulator (CFTR)-expressing airway serous cells. in The Journal of biological chemistry 2011
Show all 2 Pubmed References
Human Polyclonal SLC26A4 Primary Antibody für IHC, IHC (p) - ABIN4892725
Jia, Jiang, Dai, Xiao, Wang: Pendrin, an anion exchanger on lung epithelial cells, could be a novel target for lipopolysaccharide-induced acute lung injury mice. in American journal of translational research 2016
the evaluation of SLC26A4 CpG site methylation reflected an increased risk of presbycusis among the male participants.
Molecular analysis of human solute carrier (zeige SERTAD2 Antikörper) SLC26A2 (zeige SLC26A2 Antikörper), SLC26A3 (zeige SLC26A3 Antikörper), and SLC26A4 anion transporter disease-causing mutations using 3-dimensional homology modeling has been presented.
DFNB4 shows vestibular dysfunction, which is strongly linked to hearing loss at low frequencies without any allelic or anatomical predisposing factor
We performed simultaneous hearing screening and genetic screening targeting four common deafness mutations (p.V37I and c.235delC of GJB2 (zeige GJB2 Antikörper), c.919-2A>G of SLC26A4, and the mitochondrial m.1555A>G) in 5173 newborns at a tertiary hospital between 2009 and 2015,We delineated the longitudinal auditory features of the highly prevalent GJB2 (zeige GJB2 Antikörper) p.V37I mutation on a general population basis
A range of SLC26A4 variants without a common recurrent mutation underlies SLC26A4-related hearing loss in Turkey, Iran, and Mexico.
a later onset of hearing loss is usually related to EVA, in absence of SLC26A4 gene mutations
A novel SLC26A4 point mutation is associated with enlarge vestibular aqueduct syndrome.
results demonstrate that 19.2% patients with nonsyndromic deafness were caused by mutations in three common deafness genes (GJB2 (zeige GJB2 Antikörper), SLC26A4 and 12S rRNA) in our northern China patient group
we hypothesize that SLC26A4 coding mutations are genetic causes for nonsyndromic hearing impairment in patients bearing heterozygous GJB2 (zeige GJB2 Antikörper) 35delG mutations.
Ears with EVA and zero or one mutant allele of SLC26A4 have less severe hearing loss, no difference in prevalence of fluctuation, and a lower prevalence of cochlear implantation in comparison to ears with two mutant alleles of SLC26A4.
Acute genetic ablation of pendrin lowers blood pressure.
Data, including data from studies using transgenic mice, suggest that over-expression of IL4 (interleukin 4) in thyroid tissue/cells up-regulates expression of Duox1 (dual oxidase 1), Duoxa1 (dual oxidase maturation factor 1), and Slc26a4 (pendrin) in thyroid tissue/cells; expression of Slc5a5 (sodium-iodide symporter) is down-regulated.
Study showed that early re-induction of Slc26a4 expression can prevent fluctuation of hearing in our Slc26a4-insufficient mouse model. Restoration of SLC26A4 expression and function could reduce or prevent fluctuation of hearing in enlargement of the vestibular aqueduct patients.
decreased plasma K(+) levels promote pendrin induction by aldosterone, which, in concert with Na(+)-Cl(-) cotransporter (zeige SLC12A3 Antikörper), counteracts the progression of hypokalemia but promotes hypertension in primary aldosterone excess.
The strial dysfunction and degeneration are the primary causes of irreversible progressive hearing loss in our Slc26a4-insufficient mouse model of vestibular aqueduct syndrome.
The Role of Epithelial Sodium Channel ENaC (zeige SCNN1A Antikörper) and the Apical Cl-/HCO3- Exchanger Pendrin in Compensatory Salt Reabsorption in the Setting of Na-Cl Cotransporter (NCC (zeige SLC12A3 Antikörper)) Inactivation.
Pendrin is expressed in the adrenal medulla, where it blunts stress-induced catecholamine release.
Pendrin gene ablation reduced ENaC (zeige SCNN1A Antikörper)-mediated Na(+) absorption by reducing channel open probability as well as by reducing channel density through changes in subunit total protein abundance and subcellular distribution.
The result provides insight into the role of Na+ transport in the development and regulation of endolymphatic hydrops due to pendrin mutations.
Insufficient availability of thyroid hormone (zeige PTH Antikörper) during inner ear development plays an important role in the mechanism underlying deafness as a result of SLC26A4 mutations.
Mutations in this gene are associated with Pendred syndrome, the most common form of syndromic deafness, an autosomal-recessive disease. It is highly homologous to the SLC26A3 gene\; they have similar genomic structures and this gene is located 3' of the SLC26A3 gene. The encoded protein has homology to sulfate transporters.
Pendred syndrome homolog
, sodium-independent chloride/iodide transporter
, solute carrier family 26, member 4
, Pendred's syndrome