Browse our anti-Solute Carrier Family 26, Member 4 (SLC26A4) Antibodies

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anti-Solute Carrier Family 26, Member 4 Antibodies (SLC26A4)
On are 27 Solute Carrier Family 26, Member 4 (SLC26A4) Antibodies from 8 different suppliers available. Additionally we are shipping Solute Carrier Family 26, Member 4 Kits (10) and Solute Carrier Family 26, Member 4 Proteins (7) and many more products for this protein. A total of 46 Solute Carrier Family 26, Member 4 products are currently listed.
DFNB4, EVA, PDS, pendrin, TDH2B
list all antibodies Gene Name GeneID UniProt
SLC26A4 29440 Q9R154
SLC26A4 5172 O43511
SLC26A4 23985 Q9R155

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Top referenced anti-Solute Carrier Family 26, Member 4 Antibodies

  1. Human Polyclonal SLC26A4 Primary Antibody for 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 (PubMed)
    Show all 2 references for 562168

  2. Cow (Bovine) Polyclonal SLC26A4 Primary Antibody for IHC, WB - ABIN2776965 : Nakao, Kanaji, Ohta, Matsushita, Arima, Yuyama, Yamaya, Nakayama, Kubo, Watanabe, Sagara, Sugiyama, Tanaka, Toda, Hayashi, Inoue, Hoshino, Shiraki, Inoue, Suzuki, Aizawa, Okinami, Nagai, Hasegawa, Fukuda, Green, Izuhara: Identification of pendrin as a common mediator for mucus production in bronchial asthma and chronic obstructive pulmonary disease. in Journal of immunology (Baltimore, Md. : 1950) 2008 (PubMed)

  3. Human Polyclonal SLC26A4 Primary Antibody for 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 (PubMed)

More Antibodies against Solute Carrier Family 26, Member 4 Interaction Partners

Human Solute Carrier Family 26, Member 4 (SLC26A4) interaction partners

  1. A novel SLC26A4 point mutation is associated with enlarge vestibular aqueduct syndrome.

  2. results demonstrate that 19.2% patients with nonsyndromic deafness were caused by mutations in three common deafness genes (GJB2 (show GJB2 Antibodies), SLC26A4 and 12S rRNA) in our northern China patient group

  3. we hypothesize that SLC26A4 coding mutations are genetic causes for nonsyndromic hearing impairment in patients bearing heterozygous GJB2 (show GJB2 Antibodies) 35delG mutations.

  4. 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.

  5. These studies implicate the involvement of pendrin-facilitated chloride-bicarbonate exchange in the regulation of airway surface liquid volume and suggest the utility of pendrin inhibitors in inflammatory lung diseases.

  6. data suggest that many patients with SLC26A4 mutations have significant residual hearing at birth, and that the hearing deterioration in these patients occurs before 3 years of age. After age 3 years, the residual hearing was relatively stable and did not tend to deteriorate

  7. Familial enlarged vestibular aqueduct can demonstrate a variety of atypical segregation patterns. Pseudodominant inheritance of SLC26A4 mutations or recessive alleles of other hearing loss genes may be more likely to occur in families in which deaf individuals have intermarried.

  8. The prevalence of SLC26A4 pathogenic variants was 4% among studied Chinese patients with congenital hypothyroidism. Our study expanded the SLC26A4 mutation spectrum, provided the best estimation of SLC26A4 mutation rate for Chinese CH patients and indicated the rarity of Pendred syndrome as a cause of congenital hypothyroidism.

  9. patients with impaired pendrin function are likely to be resistant to high blood pressure due to enhanced urinary Na(+) /Cl(-) excretion. These results suggest that pendrin may regulate blood pressure through increased urinary salt excretion.

  10. Result of molecular genetic studies, four out of the 20 patients were found to carry six recessive mutations of the SLC26A4 gene in the compound heterozygous and one such gene in the homozygous state which confirmed the hereditary nature of Pendred syndrome in the Russian population.

Mouse (Murine) Solute Carrier Family 26, Member 4 (SLC26A4) interaction partners

  1. 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.

  2. decreased plasma K(+) levels promote pendrin induction by aldosterone, which, in concert with Na(+)-Cl(-) cotransporter (show SLC12A3 Antibodies), counteracts the progression of hypokalemia but promotes hypertension in primary aldosterone excess.

  3. The strial dysfunction and degeneration are the primary causes of irreversible progressive hearing loss in our Slc26a4-insufficient mouse model of vestibular aqueduct syndrome.

  4. The Role of Epithelial Sodium Channel ENaC (show SCNN1A Antibodies) and the Apical Cl-/HCO3- Exchanger Pendrin in Compensatory Salt Reabsorption in the Setting of Na-Cl Cotransporter (NCC (show SLC12A3 Antibodies)) Inactivation.

  5. Pendrin is expressed in the adrenal medulla, where it blunts stress-induced catecholamine release.

  6. Pendrin gene ablation reduced ENaC (show SCNN1A Antibodies)-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.

  7. The result provides insight into the role of Na+ transport in the development and regulation of endolymphatic hydrops due to pendrin mutations.

  8. Insufficient availability of thyroid hormone (show PTH Antibodies) during inner ear development plays an important role in the mechanism underlying deafness as a result of SLC26A4 mutations.

  9. Together these data suggest that pertussis toxin contributes to pertussis pathology through the upregulation of pendrin, which promotes conditions favoring inflammatory pathology.

  10. Using a transgenic mouse line in which all Slc26a4 expression was under the control of doxycycline, showed that fluctuations of hearing result from fluctuations of endocochlear potential and stria vascularis dysfunction in Slc26a4-insufficient mouse ears

Solute Carrier Family 26, Member 4 (SLC26A4) Antigen Profile

Antigen Summary

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.

Alternative names and synonyms associated with Solute Carrier Family 26, Member 4 (SLC26A4)

  • solute carrier family 26, member 4 (SLC26A4) antibody
  • solute carrier family 26 (anion exchanger), member 4 (Slc26a4) antibody
  • solute carrier family 26 (anion exchanger), member 4 (SLC26A4) antibody
  • solute carrier family 26, member 4 (Slc26a4) antibody
  • DFNB4 antibody
  • EVA antibody
  • PDS antibody
  • pendrin antibody
  • TDH2B antibody

Protein level used designations for SLC26A4

Pendred syndrome homolog , pendrin , sodium-independent chloride/iodide transporter , solute carrier family 26, member 4 , Pendred's syndrome

100060222 Equus caballus
29440 Rattus norvegicus
5172 Homo sapiens
23985 Mus musculus
483263 Canis lupus familiaris
100622822 Sus scrofa
530241 Bos taurus
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