U.S. Healthcare Personnel and Influenza Vaccination During the 2004–2005 Vaccine Shortage

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• 作者：Suchita A. Lorick ; Pascale M. Wortley ; Megan C. Lindley ; Barbara H. Bardenheier ; Gary L. Euler
• 关键词：Myotendinous junctions ; ILK ; Integrin ; Laminin ; loc ; Zebrafish ; Muscular dystrophy ; MLP ; β ; -parvin
• 刊名：American Journal of Preventive Medicine
• 出版年：2008
• 出版时间：June 2008
• 年：2008
• 卷：34
• 期：6
• 页码：455-462
• 全文大小：104 K

文摘

Mechanical instability of skeletal muscle cells is the major cause of congenital muscular dystrophy. Here we show that the zebrafish lost-contact mutant, that lacks a functional integrin-linked kinase (ilk) gene, suffers from mechanical instability of skeletal muscle fibres. With genetic and morpholino knock-down experiments we demonstrate that: 1) laminin, itg7, Ilk and β-parvin are all critical for mechanical stability in skeletal muscles. 2) Ilk acts redundantly with the dystrophin/dystroglycan adhesion complex in maintaining mechanical stability of skeletal muscles. 3) Ilk protein is recruited to the myotendinous junctions, which requires the ECM component laminin and the presence of itg7 in the sarcolemma. 4) Ilk, unexpectedly, is dispensable for formation of the adhesion complex. Ilk, however, is required for strengthening the adhesion of the muscle fibre with the ECM and this activity requires the presence of a functional kinase domain in Ilk. 5) We identified a novel interaction between Ilk and the mechanical stretch sensor protein MLP. Thus, Ilk is an essential intracellular component downstream of laminin and itg7, providing strengthening of skeletal muscle fibre adhesion with the ECM and therefore qualified as a novel candidate gene for congenital muscular dystrophy.