GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.

Have any questions? Please email us at ecoliwiki@gmail.com


Jump to: navigation, search


You don't have sufficient rights on this wiki to edit tables. Perhaps you need to log in. Changes you make in the Table editor will not be saved back to the wiki

See Help for Help on this wiki. See the documentation for how to use the table editor


Nofsinger, RR, Li, P, Hong, SH, Jonker, JW, Barish, GD, Ying, H, Cheng, SY, Leblanc, M, Xu, W, Pei, L, Kang, YJ, Nelson, M, Downes, M, Yu, RT, Olefsky, JM, Lee, CH and Evans, RM (2008) SMRT repression of nuclear receptors controls the adipogenic set point and metabolic homeostasis. Proc. Natl. Acad. Sci. U.S.A. 105:20021-6


The nuclear receptor corepressor, silencing mediator of retinoid and thyroid hormone receptors (SMRT), is recruited by a plethora of transcription factors to mediate lineage and signal-dependent transcriptional repression. We generated a knockin mutation in the receptor interaction domain (RID) of SMRT (SMRT(mRID)) that solely disrupts its interaction with nuclear hormone receptors (NHRs). SMRT(mRID) mice are viable and exhibit no gross developmental abnormalities, demonstrating that the reported lethality of SMRT knockouts is determined by non-NHR transcription factors. However, SMRT(mRID) mice exhibit widespread metabolic defects including reduced respiration, altered insulin sensitivity, and 70% increased adiposity. The latter phenotype is illustrated by the observation that SMRT(mRID)-derived MEFs display a dramatically increased adipogenic capacity and accelerated differentiation rate. Collectively, our results demonstrate that SMRT-RID-dependent repression is a key determinant of the adipogenic set point as well as an integrator of glucose metabolism and whole-body metabolic homeostasis.


PubMed PMC2598729 Online version:10.1073/pnas.0811012105


Adipogenesis/genetics; Animals; Chromatin Immunoprecipitation; DNA-Binding Proteins/genetics; DNA-Binding Proteins/metabolism; Down-Regulation; Gene Expression Regulation; Gene Knock-In Techniques; Genes, Lethal; Glucose/metabolism; Homeostasis/genetics; Mice; Mice, Mutant Strains; Nuclear Receptor Co-Repressor 2; PPAR gamma/metabolism; Protein Structure, Tertiary; Repressor Proteins/genetics; Repressor Proteins/metabolism; Thyroid Hormone Receptors alpha/genetics; Thyroid Hormone Receptors beta/genetics; Thyroid Hormones/metabolism