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SLC10A2 Antibody (C-term) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | Q12908 |
|---|---|
| Clone Names | 100311260 |
| Gene ID | 6555 |
|---|---|
| Other Names | Ileal sodium/bile acid cotransporter, Apical sodium-dependent bile acid transporter, ASBT, Ileal Na(+)/bile acid cotransporter, Ileal sodium-dependent bile acid transporter, IBAT, ISBT, Na(+)-dependent ileal bile acid transporter, Sodium/taurocholate cotransporting polypeptide, ileal, Solute carrier family 10 member 2, SLC10A2, ASBT, ISBT, NTCP2 |
| Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
| Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
| Name | SLC10A2 |
|---|---|
| Synonyms | ASBT, ISBT, NTCP2 |
| Function | Plays a critical role in the sodium-dependent reabsorption of bile acids from the lumen of the small intestine (PubMed:7592981, PubMed:9458785, PubMed:9856990). Transports various bile acids, unconjugated or conjugated, such as cholate and taurocholate (PubMed:7592981, PubMed:9458785, PubMed:9856990). Also responsible for bile acid transport in the renal proximal tubules, a salvage mechanism that helps conserve bile acids (Probable). Works collaboratively with the Na(+)-taurocholate cotransporting polypeptide (NTCP), the organic solute transporter (OST), and the bile salt export pump (BSEP), to ensure efficacious biological recycling of bile acids during enterohepatic circulation (PubMed:33222321). |
| Cellular Location | Membrane; Multi-pass membrane protein. |
| Tissue Location | Mainly expressed in ileum and kidney, lower expression in cecum. |
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Provided below are standard protocols that you may find useful for product applications.
Background
This gene encodes a sodium/bile acid cotransporter. Thistransporter is the primary mechanism for uptake of intestinal bileacids by apical cells in the distal ileum. Bile acids are thecatabolic product of cholesterol metabolism, so this protein isalso critical for cholesterol homeostasis. Mutations in this genecause primary bile acid malabsorption (PBAM); muatations in thisgene may also be associated with other diseases of the liver andintestines, such as familial hypertriglyceridemia (FHTG). [providedby RefSeq].
References
Halpern, M.D., et al. Am. J. Physiol. Gastrointest. Liver Physiol. 299 (3), G623-G631 (2010) :Zheng, X., et al. Int J Pharm 396 (1-2), 111-118 (2010) :Liu, C.Y., et al. Carcinogenesis 31(7):1259-1263(2010)Roberts, K.E., et al. Gastroenterology 139(1):130-139(2010)Edenberg, H.J., et al. Alcohol. Clin. Exp. Res. 34(5):840-852(2010)
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