Anti-Bile Acid Receptor NR1H4 antibody (ab28480)

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Overview

Properties

Applications

Our Abpromise guarantee covers the use of ab28480 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
WB 1/500. Detects a band of approximately 55 kDa (predicted molecular weight: 55 kDa).Can be blocked with Mouse Bile Acid Receptor NR1H4 peptide (ab39820).

Target

  • Function
    Ligand-activated transcription factor. Receptor for bile acids such as chenodeoxycholic acid, lithocholic acid and deoxycholic acid. Represses the transcription of the cholesterol 7-alpha-hydroxylase gene (CYP7A1) through the induction of NR0B2 or FGF19 expression, via two distinct mechanisms. Activates the intestinal bile acid-binding protein (IBABP). Activates the transcription of bile salt export pump ABCB11 by directly recruiting histone methyltransferase CARM1 to this locus.
  • Sequence similarities
    Belongs to the nuclear hormone receptor family. NR1 subfamily.
    Contains 1 nuclear receptor DNA-binding domain.
  • Cellular localization
    Nucleus.
  • Information by UniProt
  • Database links
    see all
  • Alternative names
    • BAR antibody
    • Bile acid receptor antibody
    • Farnesoid X activated receptor antibody
    • Farnesoid X receptor antibody
    • Farnesoid X-activated receptor antibody
    • Farnesol receptor HRR 1 antibody
    • Farnesol receptor HRR-1 antibody
    • Farnesol receptor HRR1 antibody
    • FXR antibody
    • HRR 1 antibody
    • HRR1 antibody
    • NR1H4 antibody
    • NR1H4_HUMAN antibody
    • Nuclear receptor subfamily 1 group H member 4 antibody
    • Retinoid X receptor interacting protein 14 antibody
    • Retinoid X receptor-interacting protein 14 antibody
    • RIP 14 antibody
    • RIP14 antibody
    • RXR interacting protein 14 antibody
    • RXR-interacting protein 14 antibody
    see all

References

ab28480 has not yet been referenced specifically in any publications.

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