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- W76218495 abstract "Alterations in cell shape or substrate adhesion often accompany changes in the expression and/or distribution of proteins that influence cellular architecture; these include structural elements which comprise the extracellular matrix (ECM), their transmembrane receptors (integrins) as well as components of the focal adhesion sites (focal contacts) (Spiegelman and Farmer, 1982; Ben-Ze’ev, 1986; Ben-Ze’ev, 1987; Dike and Farmer, 1988; Rodriguez et al., 1989; Dalton et al., 1992). Modulation of cell morphology and adhesivity may be a direct consequence of specific perturbations within the actin cytoskeleton. The actin-based microfilament network undergoes dramatic reorganization after exposure of cells to transforming retroviruses (Altenburg et al., 1976; Wang and Goldberg, 1976), growth factors (Bockus and Stiles, 1984; Herman and Pledger, 1985; Ridley and Hall, 1992) and microfilament-disrupting agents such as the cytochalasins (Goodman and Miranda, 1978; Schliwa, 1982; Cooper, 1987). Such induced architectural changes frequently signal specific changes in gene expression and cell growth behavior. In normal rat kidney (NRK) cells, for example, actin reorganization (associated with transformation by retroviral oncogenes or cell shape-modulating drugs) is typically reflected in morphologic restructuring, in reduced substrate adhesion and in the reprogramming of gene expression (Ryan and Higgins, 1988, 1989, 1991; Higgins and Ryan, 1989a, 1989b; Higgins et al., 1991). One gene which appears particularly susceptible to shape-associated expression in the NRK cell system encodes the 52-kDa type-1 inhibitor of plasminogen activator [p52(PAI-1)]." @default.
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- W76218495 date "1994-01-01" @default.
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- W76218495 title "Control of p52(PAI-1) Gene Expression in Normal and Transformed Rat Kidney Cells: Relationship between p52(PAI-1) Induction and Actin Cytoarchitecture" @default.
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- W76218495 doi "https://doi.org/10.1007/978-1-4615-2578-3_20" @default.
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