anti-Organic Solute Transporter alpha (OSTALPHA) 抗体

Human Organic Solute Transporter alpha (OSTALPHA) interaction partners

1. SLC51A expression is significantly upregulated in human masticatory mucosa during wound healing

2. Hepatic OSTalpha-OSTbeta expression is induced by hypoxia.

3. Ostbeta is required for both proper trafficking of Ostalpha and formation of the functional transport unit, and identify specific residues of Ostbeta critical for these processes.

4. The present report summarizes the evidence for a pleiotropic role of Ostalpha-Ostbeta in different tissues.

5. OSTalpha has roles in biological transport and is widely expressed in human tissues

6. overexpression of human OSTalpha and OSTbeta facilitated the uptake of conjugated chenodeoxycholate and the activation of FXR target genes

7. OSTalpha/OSTbeta expression is induced by bile acids through ligand-dependent transactivation of both OST genes by the nuclear bile acid receptor/farnesoid X receptor (FXR).

8. the selective localization of OSTalpha and OSTbeta to the basolateral plasma membrane of epithelial cells responsible for bile acid and sterol reabsorption.

9. These results indicate that expression of Ostalpha and Ostbeta are highly regulated in response to cholestasis and that this response is dependent on the FXR bile acid receptor.

10. Demonstrate association of OST-alpha and OST-beta to determine trafficking to plasma membrane and activity.

11. The mRNA expression of OSTalpha-OSTbeta was significantly reduced (OSTalpha: 3.3-fold, P = 0.006; OSTbeta: 2.6-fold, P = 0.03) in normal-weight but not overweight gallstone carriers

12. human OSTalpha is a glycoprotein that requires interaction with OSTbeta to reach the plasma membrane. However, glycosylation of OSTalpha is not necessary for interaction with the beta subunit or for membrane localization .

Mouse (Murine) Organic Solute Transporter alpha (OSTALPHA) interaction partners

1. Data suggest that transport of bile acid taurocholate is retained when OstB (organic solute transporter beta subunit) is truncated to contain only the transmembrane domain with 15 additional residues on each side and co-expressed with intact OstA; shorter fragments of OstB are inactive.

2. These findings indicate that loss of OSTalpha protects against age-related weight gain and insulin resistance.

3. Ileal FGF15 expression was directly correlated with plasma cholesterol levels and aortic cholesterol content. In contrast, plasma and hepatic cholesterol levels and atherosclerosis development were not reduced in apoE(-/-) mice deficient in Ostalpha.

4. Total ileal FGF15 expression was elevated almost 20-fold in Ostalpha(-/-) mice as a result of increased villus epithelial cell number and ileocyte FGF15 protein expression

5. Inactivation of FXR largely unmasked the bile acid malabsorption phenotype and corrected the bile acid homeostasis defect in Ostalpha null mice.

6. Ostalpha-deficient mice efficiently eliminate excess bile acids via the feces.

7. OSTalpha is localized to steroidogenic cells of the brain and adrenal gland, and it modulates DHEA/DHEAS homeostasis

8. These findings indicate that loss of Ostalpha provides protection from liver injury in obstructive cholestasis through adaptive responses in both the kidney and liver that enhance clearance of bile acids into urine.

9. Co-expression of mouse Ostalpha-Ostbeta, but not the individual subunits, stimulated Na(+)-independent bile acid uptake and the apical-to-basolateral transport of taurocholate

10. OSTalpha and OSTbeta mRNA levels were induced in the adrenals and kidneys of wild-type, but not FXR-/-, mice

11. the selective localization of OSTalpha and OSTbeta to the basolateral plasma membrane of epithelial cells responsible for bile acid and sterol reabsorption.

12. In conclusion, we identified Ost-alpha/Ost-beta as a novel FXR target. Absent Ost-alpha/Ost-beta induction in CA-fed FXR(-/-) animals may contribute to increased liver injury in these animals.

13. The mouse Ostalpha and Ostbeta promoters are unusual in that they contain functional FXR and LRH elements, which mediate, respectively, positive and negative feedback regulation by bile acids.

14. These results indicate that expression of Ostalpha and Ostbeta are highly regulated in response to cholestasis and that this response is dependent on the FXR bile acid receptor.

15. LXRalpha transcriptionally regulate mouse organic solute transporter alpha/beta via inverted repeat-1 elements shared with farnesoid X receptor

16. Present as heterodimers (with Ost beta) and/or heteromultimers; the interaction between Ostalpha and Ostbeta increases the stability of the proteins and is required for delivery of the heteromeric complex to the plasma membrane.

17. These data indicate that Ostalpha-Ostbeta is essential for intestinal bile acid transport in mice.

18. These findings provide direct support for the hypothesis that Ostalpha-Ostbeta is a major basolateral transporter of bile acids and conjugated steroids in the intestine, kidney, and liver.