Journal
DEVELOPMENTAL CELL
Volume 2, Issue 6, Pages 721-731Publisher
CELL PRESS
DOI: 10.1016/S1534-5807(02)00187-9
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Funding
- NIDDK NIH HHS [P01 DK57743, R01 DK53366] Funding Source: Medline
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The orphan nuclear hormone receptor SHP has been proposed to have a key role in the negative feedback regulation of bile acid production. Consistent with this, mice lacking the SHP gene exhibit mild defects in bile acid homeostasis and fail to repress cholesterol 7-alpha-hydroxylase expression in response to a specific agonist for the bile acid receptor FXR. However, this repression is retained in SHP null mice fed bile acids, demonstrating the existence of compensatory repression pathways of bile acid signaling. We provide evidence for two such pathways, based on activation of the xenobiotic receptor PXR or the c-Jun N-terminal kinase JNK. We conclude that redundant mechanisms regulate this critical aspect of cholesterol homeostasis.
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