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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Solute carrier family 10

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). [provided by RefSeq, Mar 2010] (from NCBI)
Top mentioned proteins: ACID, V1a, HAD, beta 2-adrenoceptor, Cholesterol 7-alpha-Hydroxylase
Papers on ASBT
Transcriptional analysis of porcine intestinal mucosa infected with Salmonella Typhimurium revealed a massive inflammatory response and disruption of bile acid absorption in ileum.
Garrido et al., Córdoba, Spain. In Vet Res, Dec 2015
Infection also down-regulated genes of the FXR pathway (e.g., NR1H4, FABP6, APOA1, SLC10A2), indicating disruption of the bile acid absorption in ileum.
Epiberberine reduces serum cholesterol in diet-induced dyslipidemia Syrian golden hamsters via network pathways involving cholesterol metabolism.
Ye et al., Chongqing, China. In Eur J Pharmacol, Dec 2015
Furthermore, the antidyslipidemia effect of epiberberine on key genes involved in cholesterol biosynthesis, uptake, conversion and elimination such as 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), low density lipoprotein receptor (LDL receptor), 7-alpha-hydroxylase (CYP7A1) and apical sodium dependent bile acid transporter (ASBT) were investigated.
Inhibition of Intestinal Bile Acid Absorption Improves Cholestatic Liver and Bile Duct Injury in a Mouse Model of Sclerosing Cholangitis.
Trauner et al., Vienna, Austria. In J Hepatol, Dec 2015
Therefore, pharmacological inhibition of the ileal apical sodium-dependent BA transporter (ASBT/SLC10A2) may protect against BA-mediated cholestatic liver and bile duct injury.
Bile Acids Trigger GLP-1 Release Predominantly by Accessing Basolaterally Located G Protein-Coupled Bile Acid Receptors.
Reimann et al., Cambridge, United Kingdom. In Endocrinology, Nov 2015
This action has been attributed to activation of the G protein-coupled bile acid receptor GPBAR1 (TGR5), although other potential bile acid sensors include the nuclear farnesoid receptor and the apical sodium-coupled bile acid transporter ASBT.
Enhanced antitumour drug delivery to cholangiocarcinoma through the apical sodium-dependent bile acid transporter (ASBT).
Macias et al., Salamanca, Spain. In J Control Release, Nov 2015
Here we have investigated the usefulness of targeting cytostatic bile acid derivatives to enhance the delivery of chemotherapy to tumours expressing the bile acid transporter ASBT and whether this is the case for CCA.
Slc10a2-null mice uncover colon cancer-promoting actions of endogenous fecal bile acids.
Cheng et al., Atlanta, United States. In Carcinogenesis, Oct 2015
In this study, we exploited mice deficient in the ileal apical sodium-dependent bile acid transporter (ASBT, encoded by SLC10A2) in whom fecal bile acid excretion is augmented more than 10-fold.
New paradigms in the treatment of hepatic cholestasis: from UDCA to FXR, PXR and beyond.
Poupon et al., Amsterdam, Netherlands. In J Hepatol, Apr 2015
The membrane receptors fibroblast growth factor receptor 4 (FGFR4) and apical sodium BA transporter (ASBT) deserve attention as additional therapeutic targets, as does the potential therapeutic agent norUDCA, a 23-C homologue of UDCA.
Addressing unmet medical needs in type 2 diabetes: a narrative review of drugs under development.
Turner et al., Vienna, Austria. In Curr Diabetes Rev, 2014
The new drug classes described include PPAR agonists/modulators, glucokinase activators, glucagon receptor antagonists, anti-inflammatory compounds, G-protein coupled receptor agonists, gastrointestinal peptide agonists other than GLP-1, apical sodium-dependent bile acid transporter (ASBT) inhibitors, SGLT1 and dual SGLT1/SGLT2 inhibitors, and 11beta- HSD1 inhibitors.
Structural insights into the transport of small molecules across membranes.
Buchanan et al., Bethesda, United States. In Curr Opin Struct Biol, 2014
Structures of TbpA/B and HmuUV provided new insight into iron uptake by pathogenic bacteria while the structures of NarK, ASBT, and VcINDY revealed molecular details about the transport of nitrate, bile acids and dicarboxylates, respectively.
Structural basis of the alternating-access mechanism in a bile acid transporter.
Zhou et al., Houston, United States. In Nature, 2014
In humans, there are two Na(+)-dependent bile acid transporters involved in enterohepatic recirculation, the Na(+)-taurocholate co-transporting polypeptide (NTCP; also known as SLC10A1) expressed in hepatocytes, and the apical sodium-dependent bile acid transporter (ASBT; also known as SLC10A2) expressed on enterocytes in the terminal ileum.
Sodium-dependent bile salt transporters of the SLC10A transporter family: more than solute transporters.
Stieger et al., Grafton, United States. In Pflugers Arch, 2014
The SLC10A transporter gene family consists of seven members and substrates transported by three members (SLC10A1, SLC10A2 and SLC10A6) are Na(+)-dependent.
A review of the JR blood group system.
Reid et al., Campinas, Brazil. In Immunohematology, 2012
The JR blood group system (ISBT 032) consists of one antigen,Jra, which is of high prevalence in all populations.
Evolution of substrate specificity for the bile salt transporter ASBT (SLC10A2).
Cai et al., New Haven, United States. In J Lipid Res, 2012
ASBT evolved from the earliest vertebrates by gaining affinity for modern bile salts while retaining affinity for older bile salts
Enteropathogenic Escherichia coli inhibits ileal sodium-dependent bile acid transporter ASBT.
Alrefai et al., Chicago, United States. In Am J Physiol Gastrointest Liver Physiol, 2012
This study provided novel evidence for the alterations in the activity of ASBT by enteropathogenic Escherichia coli infection.
Regulation of the gene encoding the intestinal bile acid transporter ASBT by the caudal-type homeobox proteins CDX1 and CDX2.
Eloranta et al., Zürich, Switzerland. In Am J Physiol Gastrointest Liver Physiol, 2012
The human ASBT promoter was activated transcriptionally by CDX1 and CDX2.
Functional characterization of genetic variants in the apical sodium-dependent bile acid transporter (ASBT; SLC10A2).
Kim et al., Nashville, United States. In J Gastroenterol Hepatol, 2011
Presence of multiple functionally relevant variants in SLC10A2 that may influence bile acid homeostasis and physiology.
Crystal structure of a bacterial homologue of the bile acid sodium symporter ASBT.
Drew et al., London, United Kingdom. In Nature, 2011
However, bile acids released from the bile duct are constantly recycled, being reabsorbed in the intestine by the apical sodium-dependent bile acid transporter (ASBT, also known as SLC10A2).
Effects of SLC10A2 variant rs9514089 on gallstone risk and serum cholesterol levels- meta-analysis of three independent cohorts.
Kovacs et al., Leipzig, Germany. In Bmc Med Genet, 2010
There was no significant association of rs9514089 with gallstone risk, serum lipid parameters and BMI in the Sorbs and in the meta-analysis of all three cohorts. [meta-analysis]
Bile salt transporters: molecular characterization, function, and regulation.
Boyer et al., Graz, Austria. In Physiol Rev, 2003
The bile salt pool undergoes an enterohepatic circulation that is regulated by distinct bile salt transport proteins, including the canalicular bile salt export pump BSEP (ABCB11), the ileal Na(+)-dependent bile salt transporter ISBT (SLC10A2), and the hepatic sinusoidal Na(+)- taurocholate cotransporting polypeptide NTCP (SLC10A1).
Hepatocyte nuclear factor-1alpha is an essential regulator of bile acid and plasma cholesterol metabolism.
Stoffel et al., New York City, United States. In Nat Genet, 2001
In intestine and kidneys, Tcf1-/- mice lack expression of the ileal bile acid transporter (Slc10a2), resulting in increased fecal and urinary bile acid excretion.
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