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

Mutations in SLC26A4 are associated with Pendred syndrome, the most common form of syndromic deafness, an autosomal-recessive disease. Additionally we are shipping Solute Carrier Family 26, Member 4 Antibodies (26) and Solute Carrier Family 26, Member 4 Proteins (7) and many more products for this protein.

list all ELISA KIts Gene Name GeneID UniProt
SLC26A4 29440 Q9R154
SLC26A4 5172 O43511
SLC26A4 23985 Q9R155
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Top Solute Carrier Family 26, Member 4 ELISA Kits at antibodies-online.com

Showing 3 out of 7 products:

Catalog No. Reactivity Sensitivity Range Images Quantity Supplier Delivery Price Details
Human 0.128 ng/mL 0.31-20 ng/mL 96 Tests Log in to see 9 to 11 Days
$736.84
Details
Mouse
  96 Tests Log in to see 11 to 13 Days
$875.60
Details
Rat
  96 Tests Log in to see 11 to 13 Days
$875.60
Details

More ELISA Kits for Solute Carrier Family 26, Member 4 Interaction Partners

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

  1. Mutations in RAI1 (show DOM3Z ELISA Kits), OTOF (show OTOF ELISA Kits), and SLC26A4 may have roles in nonsyndromic hearing loss in Altaian families in Siberia

  2. A homozygous c.-2071_307+3801del7666 deletion of SLC26A4 was identified in patient D1467-1. This novel genomic deletion was subsequently identified in 18% (4/22) of the Chinese Han EVA probands.

  3. GJB2 (show GJB2 ELISA Kits) and SLC26A4 mutations are associated with good post-implant outcomes.

  4. exon sequencing of GJB2 (show GJB2 ELISA Kits), SLC26A4, and mtDNA12SrRNA reveals that non-syndromic deafness in Xiamen, China appears to have a genetic etiology

  5. Anoctamin and pendrin are two plausible candidates as mediators of apical iodide efflux--{review}

  6. Data suggest that ombined hearing screening and genetic screening of gap junction protein beta 2 (GJB2 (show GJB2 ELISA Kits)), mtDNA 12srRNA and solute carrier family 26, member 4 protein SLC26A4 mutations can improve the rate of detection.

  7. Increased expression of the epithelial anion transporter pendrin/SLC26A4 in nasal polyps of patients with chronic rhinosinusitis

  8. codon 723 was a hot-spot region in SLC26A4 with a significant impact on the structure and function of pendrin, and acted as one of the genetic factors responsible for the development of hearing loss.

  9. The prevalence of SLC26A4 mutations was 12.39%, 8.84%, and 8.57% in Han Chinese, Hui people, and Tibetan participants, respectively. The c.919-2 A>G mutation was the most common form, accounting for 60.47% of all SLC26A4 mutant alleles.

  10. Presence of mono-allelic mutations of SLC26A4 in non-syndromic enlarged vestibular aqueduct patients is etiologically associated with this disorder.

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

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

  2. 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.

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

  4. 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.

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

  6. 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.

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

  8. 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

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

  10. This review summarizes recent studies in mouse models that have been developed to delineate the role of pendrin in the physiology of hearing

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.

Gene names and symbols associated with 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

GENE ID SPECIES
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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