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Stimulation of extension

However, there is also stimulation of turnover of old adhesion sites. One possible mechanism for stimulated removal of old adhesion sites is via extracellular signal-regulated kinase (ERK) activation of calpain [249], followed by calpain-mediated cleavage of adhesion proteins such [Pg.290]

Mechanisms of contraction for mesenchymal cells may be more dependent on formation of stress fibers and focal contacts than on the cortical contraction mechanisms seen in Dictyostelium [195]. Receptor tyrosine kinases can stimulate increased myosin light chain phosphorylation via rho activation as a mechanism for contraction. Alternatively, increased contraction may follow formation of new focal contacts, possibly via focal adhesion kinase and src-based mechanisms [212]. This would be consistent with the temporal sequence of events that are observed, with contraction being a late step that should follow formation of new focal contacts. [Pg.291]


See other pages where Stimulation of extension is mentioned: [Pg.289]    [Pg.244]   


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