Signals regulating adhesion dynamics.
Signals regulating adhesion dynamics.
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调节粘附动力学的信号。
DOI:
10.1155/2012/785196
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发表时间:
2012
期刊:
影响因子:
--
通讯作者:
DeMali,KrisA
中科院分区:
文献类型:
--
作者:
Webb,DonnaJ;Brown,ClaireM;DeMali,KrisA
Adhesions are sites of contact between cells (cell-cell) and between cells and the extracellular matrix (cell-ECM) that are essential for numerous biological processes such as embryogenesis, wound healing, and the immune response. They are composed of many different molecules including adhesion receptors, signaling proteins (eg, kinases, phosphatases, and adaptor proteins), and structural proteins (eg, actin-binding proteins)[1–3]. Adhesions are dynamic structures whose molecular composition and structure can undergo rapid changes to allow cells to respond to external signals [1, 4]. Indeed, this dynamic nature of adhesions within localized regions of cells is critical for many complex processes such as cell migration. For cell-ECM adhesions, their assembly is initiated by the binding of integrin adhesion receptors to the ECM. These new adhesions can either disassemble, allowing cells to migrate, or continue to mature by recruiting signaling and structural proteins to these sites. The dynamics and composition of adhesions are controlled by signaling networks that function to integrate molecular signals from outside and within cells. This special issue focuses on the molecular signals that regulate adhesion dynamics with an emphasis on cell-ECM adhesions.Integrins are transmembrane adhesion receptors that provide a functional link between the ECM and the actin cytoskeleton. Integrin engagement of the ECM serves to transduce signals to the interior of cells which regulate cell behavior. RGD-dependent integrins are a subgroup of adhesion receptors that specifically recognize the RGD motif, which is a three-amino-acid sequence (Arg-Gly-Asp) that is found in some ECM proteins. In this special issue, YD Benoit et al. review recent findings regarding the importance of RGD-dependent integrins in epithelial cell homeostasis.