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Validated All-in-One™ qPCR Primer for SLC10A1(NM_003049.3) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
Sodium/bile acid cotransporters are integral membrane glycoproteins that participate in the enterohepatic circulation of bile acids. Two homologous transporters are involved in the reabsorption of bile acids, one absorbing from the intestinal lumen, the bile duct, and the kidney with an apical localization (SLC10A2; MIM 601295), and the other being found in the basolateral membranes of hepatocytes (SLC10A1).[supplied by OMIM].
Gene References into function
- Translation/insertion scanning, alanine insertion, and glycosylation site mutagenesis studies of liver sodium/bile acid cotransporter support a topography with nine membrane-spanning or membrane-associated segments.
- a domain critical for bile acid substrate recognition of SLC10A1 has an ethnicity-dependent polymorphism
- Conserved NTCP/Ntcp 5'-regulatory region transcription regulation differs among species and is not directly regulated by small heterodimer partner. Bile acids may regulate NTCP/Ntcp indirectly by modulating nuclear factor regulation of gene expression.
- The present studies were undertaken to establish a suitable in vitro experimental model to study human ASBT function and its regulation by cholesterol.
- The major canalicular transporter genes are expressed at mid-gestational stage during human fetal development.
- Results suggest that the Ser-226 in the third cytoplasmic loop of NTCP is phosphorylated and cAMP may increase NTCP translocation to the cell membrane by dephosphorylating NTCP at this site.
- The GR/dexamethasone activation of the hNTCP promoter is counteracted by bile acids and small heterodimer partner, providing a negative feedback mechanism for bile acid uptake in human hepatocytes.
- Cholesterol treatment led to increased levels of NTCP and OCT-1 mRNAs.