SLC10A2

Jump to: navigation, search
VALUE_ERROR (nil)
Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

n/a

n/a

RefSeq (protein)

n/a

n/a

Location (UCSC)n/an/a
PubMed searchn/an/a
Wikidata
View/Edit Human

The SLC10A2 (solute carrier family 10 member 2) gene in humans encodes the bile acid:sodium symporter known as the apical sodium–bile acid transporter (ASBT) or as the ileal bile acid transporter (IBAT).[1][2]

ASBT/IBAT is most highly expressed in the ileum, where it is found on the brush border membrane of enterocytes. It is responsible for the initial uptake of bile acids, particularly conjugated bile acids, from the intestine as part of their enterohepatic circulation.[3]

As a drug target

Several medications to inhibit IBAT are under development. They include elobixibat, under development for the treatment of constipation and irritable bowel syndrome,[4] and volixibat, under development for the treatment of nonalcoholic steatohepatitis.[5]

See also

References

  1. Wong MH, Rao PN, Pettenati MJ, Dawson PA (May 1996). "Localization of the ileal sodium-bile acid cotransporter gene (SLC10A2) to human chromosome 13q33". Genomics. 33 (3): 538–40. doi:10.1006/geno.1996.0233. PMID 8661017.
  2. "Entrez Gene: SLC10A2 solute carrier family 10 (sodium/bile acid cotransporter family), member 2".
  3. Dawson PA (2011). "Role of the intestinal bile acid transporters in bile acid and drug disposition". Handbook of Experimental Pharmacology (201): 169–203. doi:10.1007/978-3-642-14541-4_4. PMC 3249407. PMID 21103970.
  4. Acosta A, Camilleri M (July 2014). "Elobixibat and its potential role in chronic idiopathic constipation". Therapeutic Advances in Gastroenterology. 7 (4): 167–75. doi:10.1177/1756283X14528269. PMC 4107709. PMID 25057297.
  5. Chitnis D (2016-08-03), "FDA grants fast track status to volixibat", Internal Medicine News Digital Network, retrieved 2016-08-14.

Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.


Linked-in.jpg