Featured
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Structure of Hsp90–p23–GR reveals the Hsp90 client-remodelling mechanism
Studies based on cryo-electron microscopy structures of Hsp90 chaperone complexes reveal the molecular mechanism of the chaperone-mediated maturation of the human glucocorticoid receptor.
- Chari M. Noddings
- , Ray Yu-Ruei Wang
- & David A. Agard
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Article |
PGRMC2 is an intracellular haem chaperone critical for adipocyte function
Progesterone receptor membrane component 2 is required to transport haem from the mitochondria to the nucleus, where, in adipose tissue, it has roles in regulation of thermogenesis and glucose metabolism.
- Andrea Galmozzi
- , Bernard P. Kok
- & Enrique Saez
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Letter |
A PPARγ–FGF1 axis is required for adaptive adipose remodelling and metabolic homeostasis
PPARγ induces fibroblast growth factor 1 to remodel visceral adipose tissue in response to a high-fat diet to maintain metabolic homeostasis.
- Johan W. Jonker
- , Jae Myoung Suh
- & Ronald M. Evans
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Letter |
Cryptochromes mediate rhythmic repression of the glucocorticoid receptor
Circadian co-regulators cryptochrome 1 and 2 are shown to alter globally the transcriptional response to glucocorticoids in mouse embryonic fibroblasts.
- Katja A. Lamia
- , Stephanie J. Papp
- & Ronald M. Evans
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Letter |
A nuclear-receptor-dependent phosphatidylcholine pathway with antidiabetic effects
- Jae Man Lee
- , Yoon Kwang Lee
- & David D. Moore
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Article |
Anti-diabetic drugs inhibit obesity-linked phosphorylation of PPARγ by Cdk5
PPARγ ligands are used to control diabetes, but their anti-diabetic actions are puzzling. Here the authors show that phosphorylation of PPARγ by cyclin-dependent kinase 5 (Cdk5) in mice is linked to obesity induced by high-fat feeding, and that inhibition of the effect in humans by the drug rosiglitazone is closely associated with its anti-diabetic effects. Several anti-diabetic PPARγ ligands directly inhibit the effect, and thus support a more normal non-diabetic pattern of gene expression.
- Jang Hyun Choi
- , Alexander S. Banks
- & Bruce M. Spiegelman
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Letter |
IκBζ regulates TH17 development by cooperating with ROR nuclear receptors
Interleukin-17-producing helper T (TH17) cells are a distinct T-cell subset characterized by its role in autoimmune disease. Here it is shown that the development of TH17 cells requires the transcription factor IκBζ, as well as nuclear receptors of the ROR family. Mice lacking IκBζ have a defect in TH17 development and are resistant to the induction of experimental autoimmune encephalomyelitis. The study points to some new potential molecular targets for drugs to treat autoimmune disease.
- Kazuo Okamoto
- , Yoshiko Iwai
- & Hiroshi Takayanagi