کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10766333 | 1050646 | 2009 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Skp2 promotes adipocyte differentiation via a p27Kip1-independent mechanism in primary mouse embryonic fibroblasts
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Skp2, the substrate-binding subunit of an SCF ubiquitin ligase complex, is a key regulator of cell cycle progression that targets substrates for degradation by the 26S proteasome. We have now shown that ablation of Skp2 in primary mouse embryonic fibroblasts (MEFs) results both in impairment of adipocyte differentiation and in the accumulation of the cyclin-dependent kinase inhibitor p27Kip1, a principal target of the SCFSkp2 complex. Genetic ablation of p27Kip1 in MEFs promoted both lipid accumulation and adipocyte-specific gene expression. However, depletion of p27Kip1 by adenovirus-mediated RNA interference failed to correct the impairment of adipocyte differentiation in Skp2-/- MEFs. In contrast, troglitazone, a high-affinity ligand for peroxisome proliferator-activated receptor γ (PPARγ), largely restored lipid accumulation and PPARγ gene expression in Skp2â/â MEFs. Our data suggest that Skp2 plays an essential role in adipogenesis in MEFs in a manner that is at least in part independent of regulation of p27Kip1 expression.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 379, Issue 2, 6 February 2009, Pages 249-254
Journal: Biochemical and Biophysical Research Communications - Volume 379, Issue 2, 6 February 2009, Pages 249-254
نویسندگان
Mitsuru Okada, Tamon Sakai, Takehiro Nakamura, Mimi Tamamori-Adachi, Shigetaka Kitajima, Yasushi Matsuki, Eijiro Watanabe, Ryuji Hiramatsu, Hiroshi Sakaue, Masato Kasuga,