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SLC10A2 encodes a sodium/bile acid cotransporter. Additionally we are shipping Solute Carrier Family 10 (Sodium/bile Acid Cotransporter Family), Member 2 Antibodies (69) and many more products for this protein.
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Human SLC10A2 Protein expressed in Wheat germ - ABIN1330485
Al-Hilal, Park, Alam, Chung, Park, Kim, Kwon, Kim, Kim, Byun: Oligomeric bile acid-mediated oral delivery of low molecular weight heparin. in Journal of controlled release : official journal of the Controlled Release Society 2014
Two single-nucleotide polymorphisms at novel loci, rs112404845 (P = 3.8 x 10-8), upstream of COBL, and rs16961023 (P = 4.6 x 10-8), downstream of SLC10A2, obtained genome-wide significant evidence of association with the posterior liability of late-onset Alzheimer's disease in African Americans.
Data (including data from studies in knockout/transgenic mice) suggest that SLC10A2 is a functional receptor for hepatitis D virus in hepatocytes.
Results unravel novel roles for N-glycosylation of ASBT and suggest that high levels of glucose alter the composition of the glycan and may contribute to the increase in ASBT function in diabetes mellitus.
The p.Ser267Phe NTCP (show SLC10A1 Proteins) variant is significantly associated with resistance to chronic hepatitis B and a lower incidence of acute-on-chronic liver failure. Our results support that NTCP (show SLC10A1 Proteins) is a cellular receptor for HBV in human infection
Data indicate that the lipid flippase (ATP8B1 (show ATP8B1 Proteins))-transmembrane protein 30A (CDC50A) heterodimer is essential for the apical localization of sodium-dependent bile acid transporter (SLC10A2/ASBT) in Caco-2 cells.
It was conclude that regulation of ASBT expression by resveratrol (RSV) may have clinical relevance with regard to the observed cholesterol-lowering effects of RSV.
Transmembrane domain II of the human bile acid transporter SLC10A2 coordinates sodium translocation.
ASBT evolved from the earliest vertebrates by gaining affinity for modern bile salts while retaining affinity for older bile salts
This study provided novel evidence for the alterations in the activity of ASBT by enteropathogenic Escherichia coli infection.
Presence of multiple functionally relevant variants in SLC10A2 that may influence bile acid homeostasis and physiology.
data support the concept that under physiological conditions microbiota stimulate Gata4 (show GATA4 Proteins), which suppresses Asbt expression
In Asbt-deficient mice, the lack of bile acid uptake in the distal small intestine, which we recently documented using novel in vivo imaging results in more than 10-fold increased fecal bile acids
ileal ASBT protein is degraded by a ubiquitin-dependent pathway in response to enterobacteria-associated bile acids
Ileal Fibroblast Growth Factor-15 (FGF15) expression was significantly reduced in Asbt(-/-)apoE (show APOE Proteins)(-/-) mice and was inversely correlated with expression of hepatic cholesterol 7-hydroxylase (Cyp7a1 (show CYP7A1 Proteins)).
The functional importance of proline and uncharged polar residues in the highly conserved region of mouse Slc10a2 was determined.
Enterobacteria-mediated bile acid biotransformation modulates intestinal bile acid transport via downregulation of SLC10A2 expression.
These data confirm that bile acids and upregulation of ASBT play a crucial role in NEC pathogenesis and suggest that inhibition of ASBT could be utilized as a therapeutic modality against this disease.
Slc10a2 is essential for efficient intestinal absorption of bile acids
ASBT-mediated bile salt uptake in the distal ileum might also modulate intestinal fluid secretion
The C51A and C106A mutants of Slc10a2 showed significantly reduced TCA uptake, while no apparent difference in TCA uptake was observed for the Slc10a1-C44A mutant.
This gene encodes a sodium/bile acid cotransporter. This transporter is the primary mechanism for uptake of intestinal bile acids by apical cells in the distal ileum. Bile acids are the catabolic product of cholesterol metabolism, so this protein is also critical for cholesterol homeostasis. Mutations in this gene cause primary bile acid malabsorption (PBAM)\; muatations in this gene may also be associated with other diseases of the liver and intestines, such as familial hypertriglyceridemia (FHTG).
solute carrier family 10 (sodium/bile acid cotransporter family), member 2
, ileal sodium/bile acid cotransporter
, Na(+)-dependent ileal bile acid transporter
, apical sodium-dependent bile acid transporter
, ileal Na(+)/bile acid cotransporter
, ileal sodium-dependent bile acid transporter
, sodium/taurocholate cotransporting polypeptide, ileal
, solute carrier family 10 member 2
, sodium/taurocholate-cotransporting polypeptide, ileal
, solute carrier family 10, member 2
, ileal apical sodium-dependent bile acid transporter