Journal
MOLECULAR ENDOCRINOLOGY
Volume 20, Issue 5, Pages 1138-1152Publisher
OXFORD UNIV PRESS INC
DOI: 10.1210/me.2005-0407
Keywords
-
Categories
Funding
- NIDDK NIH HHS [DK59820] Funding Source: Medline
Ask authors/readers for more resources
Members of the steroid receptor coactivator (SRC) family, which include SRC-1 (NcoA-1/p160), SRC2(TIF2/GRIP1/NcoA-2) and SRC-3(pCIP/RAC3/ACTR/pCIP/AIB1/TRAM1), are critical mediators of steroid receptor action. Gene ablation studies previously identified SRC-1 and SRC-2 as being involved in the control of energy homeostasis. A more precise identification of the molecular pathways regulated by these coactivators is crucial for understanding the role of steroid receptor coactivators in the control of energy homeostasis and obesity. A genomic approach using microarray analysis was employed to identify the subsets of genes that are altered in the livers of SRC-1(-/-), SRC-2(-/-), and SRC-3(-/-) mice. Microarray analysis demonstrates that gene expression changes are specific and nonoverlapping for each SRC member in the liver. The overall pattern of altered gene expressions in the SRC-1(-/-) mice was upregulation, whereas SRC-2(-/-) mice showed an overall down-regulation. Several key regulatory enzymes of energy metabolism were significantly altered in the liver of SRC-2(-/-) mice, which are consistent with the prior observation that SRC2(-/-) mice have increased energy expenditure. This study demonstrates that the molecular targets of SRC-2 regulation in the murine liver stimulate fatty acid degradation and glycolytic pathway, whereas fatty acid, cholesterol, and steroid biosynthetic pathways are down-regulated.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available