Ileal sodium/bile acid cotransporter: Difference between revisions

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* {{cite journal | vauthors = Jung D, Fried M, Kullak-Ublick GA | title = Human apical sodium-dependent bile salt transporter gene (SLC10A2) is regulated by the peroxisome proliferator-activated receptor alpha | journal = The Journal of Biological Chemistry | volume = 277 | issue = 34 | pages = 30559–66 | date = August 2002 | pmid = 12055195 | doi = 10.1074/jbc.M203511200 }}
* {{cite journal | vauthors = Jung D, Fried M, Kullak-Ublick GA | title = Human apical sodium-dependent bile salt transporter gene (SLC10A2) is regulated by the peroxisome proliferator-activated receptor alpha | journal = The Journal of Biological Chemistry | volume = 277 | issue = 34 | pages = 30559–66 | date = August 2002 | pmid = 12055195 | doi = 10.1074/jbc.M203511200 }}
* {{cite journal | vauthors = Zelcer N, Saeki T, Bot I, Kuil A, Borst P | title = Transport of bile acids in multidrug-resistance-protein 3-overexpressing cells co-transfected with the ileal Na+-dependent bile-acid transporter | journal = The Biochemical Journal | volume = 369 | issue = Pt 1 | pages = 23–30 | date = January 2003 | pmid = 12220224 | pmc = 1223054 | doi = 10.1042/BJ20021081 }}
* {{cite journal | vauthors = Zelcer N, Saeki T, Bot I, Kuil A, Borst P | title = Transport of bile acids in multidrug-resistance-protein 3-overexpressing cells co-transfected with the ileal Na+-dependent bile-acid transporter | journal = The Biochemical Journal | volume = 369 | issue = Pt 1 | pages = 23–30 | date = January 2003 | pmid = 12220224 | pmc = 1223054 | doi = 10.1042/BJ20021081 }}
* {{cite journal | vauthors = Chumakov I, Blumenfeld M, Guerassimenko O, Cavarec L, Palicio M, Abderrahim H, Bougueleret L, Barry C, Tanaka H, La Rosa P, Puech A, Tahri N, Cohen-Akenine A, Delabrosse S, Lissarrague S, Picard FP, Maurice K, Essioux L, Millasseau P, Grel P, Debailleul V, Simon AM, Caterina D, Dufaure I, Malekzadeh K, Belova M, Luan JJ, Bouillot M, Sambucy JL, Primas G, Saumier M, Boubkiri N, Martin-Saumier S, Nasroune M, Peixoto H, Delaye A, Pinchot V, Bastucci M, Guillou S, Chevillon M, Sainz-Fuertes R, Meguenni S, Aurich-Costa J, Cherif D, Gimalac A, Van Duijn C, Gauvreau D, Ouellette G, Fortier I, Raelson J, Sherbatich T, Riazanskaia N, Rogaev E, Raeymaekers P, Aerssens J, Konings F, Luyten W, Macciardi F, Sham PC, Straub RE, Weinberger DR, Cohen N, Cohen D, Ouelette G, Realson J | display-authors = 6 | title = Genetic and physiological data implicating the new human gene G72 and the gene for D-amino acid oxidase in schizophrenia | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 99 | issue = 21 | pages = 13675–80 | date = October 2002 | pmid = 12364586 | pmc = 129739 | doi = 10.1073/pnas.182412499 }}
* {{cite journal | vauthors = Chumakov I, Blumenfeld M, Guerassimenko O, Cavarec L, Palicio M, Abderrahim H, Bougueleret L, Barry C, Tanaka H, La Rosa P, Puech A, Tahri N, Cohen-Akenine A, Delabrosse S, Lissarrague S, Picard FP, Maurice K, Essioux L, Millasseau P, Grel P, Debailleul V, Simon AM, Caterina D, Dufaure I, Malekzadeh K, Belova M, Luan JJ, Bouillot M, Sambucy JL, Primas G, Saumier M, Boubkiri N, Martin-Saumier S, Nasroune M, Peixoto H, Delaye A, Pinchot V, Bastucci M, Guillou S, Chevillon M, Sainz-Fuertes R, Meguenni S, Aurich-Costa J, Cherif D, Gimalac A, Van Duijn C, Gauvreau D, Ouellette G, Fortier I, Raelson J, Sherbatich T, Riazanskaia N, Rogaev E, Raeymaekers P, Aerssens J, Konings F, Luyten W, Macciardi F, Sham PC, Straub RE, Weinberger DR, Cohen N, Cohen D, Ouelette G, Realson J | display-authors = 6 | title = Genetic and physiological data implicating the new human gene G72 and the gene for D-amino acid oxidase in schizophrenia | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 99 | issue = 21 | pages = 13675–80 | date = October 2002 | pmid = 12364586 | pmc = 129739 | doi = 10.1073/pnas.182412499 | url = https://repub.eur.nl/pub/5910/eur_duijn_121.pdf }}
* {{cite journal | vauthors = Neimark E, Chen F, Li X, Shneider BL | title = Bile acid-induced negative feedback regulation of the human ileal bile acid transporter | journal = Hepatology | volume = 40 | issue = 1 | pages = 149–56 | date = July 2004 | pmid = 15239098 | doi = 10.1002/hep.20295 }}
* {{cite journal | vauthors = Neimark E, Chen F, Li X, Shneider BL | title = Bile acid-induced negative feedback regulation of the human ileal bile acid transporter | journal = Hepatology | volume = 40 | issue = 1 | pages = 149–56 | date = July 2004 | pmid = 15239098 | doi = 10.1002/hep.20295 }}
* {{cite journal | vauthors = Xia X, Roundtree M, Merikhi A, Lu X, Shentu S, Lesage G | title = Degradation of the apical sodium-dependent bile acid transporter by the ubiquitin-proteasome pathway in cholangiocytes | journal = The Journal of Biological Chemistry | volume = 279 | issue = 43 | pages = 44931–7 | date = October 2004 | pmid = 15304498 | doi = 10.1074/jbc.M400969200 }}
* {{cite journal | vauthors = Xia X, Roundtree M, Merikhi A, Lu X, Shentu S, Lesage G | title = Degradation of the apical sodium-dependent bile acid transporter by the ubiquitin-proteasome pathway in cholangiocytes | journal = The Journal of Biological Chemistry | volume = 279 | issue = 43 | pages = 44931–7 | date = October 2004 | pmid = 15304498 | doi = 10.1074/jbc.M400969200 }}

Revision as of 03:35, 25 October 2018

SLC10A2
Identifiers
AliasesSLC10A2, ASBT, IBAT, ISBT, NTCP2, PBAM, solute carrier family 10 member 2, Ileal bile acid transporter, PBAM1
External IDsOMIM: 601295; MGI: 1201406; HomoloGene: 390; GeneCards: SLC10A2; OMA:SLC10A2 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_000452

NM_011388

RefSeq (protein)

NP_000443

NP_035518

Location (UCSC)Chr 13: 103.04 – 103.07 MbChr 8: 5.13 – 5.16 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

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).[5][6]

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.[7]

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,[8] and volixibat, under development for the treatment of nonalcoholic steatohepatitis.[9]

See also

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000125255Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000023073Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ 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.
  6. ^ "Entrez Gene: SLC10A2 solute carrier family 10 (sodium/bile acid cotransporter family), member 2".
  7. ^ 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.
  8. ^ 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.
  9. ^ Chitnis, Deepak (2016-08-03), "FDA grants fast track status to volixibat", Internal Medicine News Digital Network, retrieved 2016-08-14. {{citation}}: Unknown parameter |name-list-format= ignored (|name-list-style= suggested) (help)

Further reading

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