1, 2 The endogenous ligand for the receptor is currently unknown. It was originally described because of its ability to induce cell cycle arrest in the G 2/M phase when overexpressed in pro-B and T cells. The G2A receptor is a G protein– coupled receptor member of the stress-inducible ovarian cancer G protein– coupled receptor 1 family that is highly expressed in lymphoid tissues and macrophages.
There were no changes in gallbladder volume. G2A −/− mice fed a lithogenic diet had rapid gallstone formation, an increased cholesterol saturation index, a 2.5-fold increase in farnesoid X receptor expression, a 5-fold increase in LXR expression, and a 90% reduction in cholesterol 7 α-hydroxylase expression in comparison with wild-type mice. Despite the increased expression of LXR, transcription of several LXR target genes was reduced.
G2A-deficient (G2A −/−) mice fed chow had a 25% reduction in biliary phosphatidylcholine content, reduced hepatic gene expression of the phosphatidylcholine transporter adenosine triphosphate– binding cassette B4, and an 8-fold increase in expression of the nuclear receptor liver X receptor (LXR). In this study, we examined the hepatobiliary effects of loss of function of G2A in mice fed either a chow or lithogenic diet. The G2A receptor is a member of the ovarian cancer G protein– coupled receptor 1 family of stress-inducible G protein– coupled receptors.
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