首页> 外文期刊>Annals of the Rheumatic Diseases: A Journal of Clinical Rheumatology and Connective Tissue Research >Cartilage-specific deletion of mTOR upregulates autophagy and protects mice from osteoarthritis
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Cartilage-specific deletion of mTOR upregulates autophagy and protects mice from osteoarthritis

机译:软骨特异的mTOR缺失可上调自噬并保护小鼠免受骨关节炎的侵害

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摘要

Objectives Mammalian target of rapamycin (mTOR) (a serine/threonine protein kinase) is a major repressor of autophagy, a cell survival mechanism. The specific in vivo mechanism of mTOR signalling in OA pathophysiology is not fully characterised. We determined the expression of mTOR and known autophagy genes in human OA cartilage as well as mouse and dog models of experimental OA. We created cartilage-specific mTOR knockout (KO) mice to determine the specific role of mTOR in OA pathophysiology and autophagy signalling in vivo.
机译:目的雷帕霉素(mTOR)(一种丝氨酸/苏氨酸蛋白激酶)的哺乳动物靶标是自噬的主要阻遏物,一种细胞存活机制。 OA病理生理学中mTOR信号转导的特定体内机制尚未完全表征。我们确定了mTOR和已知的自噬基因在人OA软骨以及实验OA的小鼠模型中的表达。我们创建了软骨特异性mTOR基因敲除(KO)小鼠,以确定mTOR在体内OA病理生理学和自噬信号转导中的特定作用。

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