Diverse Roles of Integrin Receptors in Articular Cartilage (Advances in Anatomy, Embryology and Cell Biology)
ISBN: 3540787704
Category: Technical
Tag: Science/Engineering
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Diverse Roles of Integrin Receptors in Articular Cartilage (Advances in Anatomy, Embryology and Cell Biology)
By Mehdi Shakibaei, Constanze Csaki, Ali Mobasheri
Publisher: Springer | ISBN: 3540787704 | edition 2008 | PDF | 62 pages | 14,9 mb
By Mehdi Shakibaei, Constanze Csaki, Ali Mobasheri
Publisher: Springer | ISBN: 3540787704 | edition 2008 | PDF | 62 pages | 14,9 mb
Integrins are heterodimeric integral membrane proteins made up of a and ß subunits. At least 18 a and 8 ß subunit genes have been described in mammals. Integrin family members are plasma membrane receptors involved in cell adhesion and active as intra- and extracellular signalling molecules in a variety of processes including embryogenesis, hemostasis, tissue repair, immune response and metastatic spread of tumor cells. Integrin beta 1 (ß1-integrin) the protein encoded by the ITGB1 gene (also known as CD29 and VLAB) is a multi-functional protein involved in cell-matrix adhesion, cell signalling, cellular defense, cell adhesion, protein binding, protein heterodimerization and receptor-mediated activity. It is highly expressed in the human body (17.4 times higher than the average gene in the last updated revision of the human genome). The extracellular matrix (ECM) of articular cartilage is a unique environment. Interactions between chondrocytes and the ECM regulate many biological processes important to homeostasis and repair of articular cartilage including cell attachment, growth, differentiation, and survival. The ß1-integrin family of cell surface receptors appears to play a major role in mediating cell-matrix interactions that are important in regulating these fundamental processes. Chondrocyte mechanoreceptors have been proposed to incorporate ß1-integrins and mechanosensitive ion channels which link with key ECM, cytoskeletal and signalling proteins to maintain the chondrocyte phenotype, prevent chondrocyte apoptosis and regulate chondrocyte-specific gene expression.
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