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TGR5 sequence variation in primary sclerosing cholangitis.

Johannes R Hov1, Verena Keitel, Erik Schrumpf

  • 1Norwegian PSC Research Center, Clinic for Specialized Medicine and Surgery, Oslo University Hospital Rikshospitalet, Oslo, Norway.

Digestive Diseases (Basel, Switzerland)
|June 22, 2011
PubMed
Summary
This summary is machine-generated.

Genetic variants in TGR5 (GPBAR1), a bile acid receptor, may increase susceptibility to primary sclerosing cholangitis (PSC) and ulcerative colitis (UC). Mutations were found to impair TGR5 function, suggesting a role in these inflammatory diseases.

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Area of Science:

  • Gastroenterology
  • Genetics
  • Immunology

Background:

  • TGR5 (GPBAR1) is a G-protein-coupled receptor involved in inflammatory pathways and homeostasis.
  • Primary sclerosing cholangitis (PSC) is a chronic bile duct disease linked to ulcerative colitis (UC).
  • A genetic locus near TGR5 has been associated with PSC and UC.

Purpose of the Study:

  • To investigate novel genetic variants of TGR5 in patients with PSC.
  • To determine the functional impact of identified TGR5 mutations.
  • To explore the association between TGR5 and susceptibility to PSC and UC.

Main Methods:

  • Resequencing of the TGR5 gene in 267 PSC patients and 274 healthy controls.
  • Experimental assessment of the functional effects of identified nonsynonymous mutations on TGR5.
  • Fine-mapping of the chromosome 2q35 locus in large patient cohorts.

Main Results:

  • Six nonsynonymous mutations and 16 other novel single-nucleotide polymorphisms (SNPs) in TGR5 were identified.
  • Five nonsynonymous mutations were shown to reduce or abolish TGR5 function.
  • A common TGR5 SNP was associated with PSC and UC, but linkage disequilibrium complicated gene-specific association.

Conclusions:

  • Novel TGR5 mutations can impair receptor function, offering insights into its structural biology.
  • TGR5 genetic variations may contribute to susceptibility to PSC and UC.
  • Further research is needed to confirm the role of TGR5 in PSC and UC pathogenesis.