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Browse our Solute Carrier Family 26, Member 4 (SLC26A4) ELISA Kits

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Solute Carrier Family 26, Member 4 ELISA Kits (SLC26A4)
On are 9 Solute Carrier Family 26, Member 4 (SLC26A4) ELISA Kits from 5 different suppliers available. Additionally we are shipping Solute Carrier Family 26, Member 4 Antibodies (27) and Solute Carrier Family 26, Member 4 Proteins (7) and many more products for this protein. A total of 45 Solute Carrier Family 26, Member 4 products are currently listed.
DFNB4, EVA, PDS, pendrin, TDH2B
list all ELISA KIts Gene Name GeneID UniProt
SLC26A4 29440 Q9R154
SLC26A4 5172 O43511
SLC26A4 23985 Q9R155

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

  1. We attempted to identify the genetic epidemiology of hereditary hearing loss among the Chinese Han population using next-generation sequencing The entire length of the genes GJB2, SLC26A4, and GJB3 were sequenced from 116 individuals suffering from hearing loss. In our study, SLC26A4 and GJB2 were the most frequently affected genes among the Chinese Han population with hearing loss.

  2. The results of the present study indicated that combined heterozygous mutations of the SLC264 and GJB3 (show GJB3 ELISA Kits) genes may result in severe hearing loss. These results contribute to the understanding of clinical phenotype of deaf patients carrying combined mutations in the SLC26A4 and GJB3 (show GJB3 ELISA Kits) genes.

  3. A novel splice site mutation of c.1001 + 5G > C was identified, and the novel compound heterozygote of two splice site mutations, c.1001 + 5G > C and c.919-2A > G, in the SLC26A4 gene has been linked to hearing impairment in enlarged vestibular aqueduct patients.

  4. This study revealed a novel heterozygous mutation c.2118C>A (p.C706X) compound with c.919-2A>G in SLC26A4 gene in a patient with enlarged vestibular aqueduct syndrome and family members.

  5. The heterozygous mutations of p.I188T, p.L582LfsX4 and p.E704K in SLC26A4 gene were responsible for the Large vestibular aqueduct syndrome of the affected individual.

  6. There are more than 39 deafness genes reported to cause non-syndromic hereditary hearing loss (HHL) in Iran, of which the most prevalent causative genes include GJB2, SLC26A4, MYO15A, and MYO7A. In addition, we highlight some of the more common genetic causes of syndromic HHL in Iran. [review]

  7. The SLC26A4 genotypes associated with enlarged vestibular aqueduct malformation in south Italian children with sensorineural hearing loss.

  8. Data show that 147 known pathogenic mutations were mapped on the solute carrier family 26 member 4 (pendrin) model and analyzed.

  9. Twenty-two of 156 deafness cases due to SLC26A4 mutations

  10. SLC26A4 mutation was identified in 2.02% of Chinese newborns with congenital hearing loss.

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

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

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

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

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

  5. Pendrin gene ablation reduced ENaC (show SCNN1A ELISA Kits)-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.

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

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

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

  9. 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

  10. Pendrin is expressed in platelets and is presumably regulated by SGK1 (show SGK1 ELISA Kits) and mineralocorticoids.

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

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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