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Titolo:
CYCLIC GMP-DEPENDENT PROTEIN-KINASE IS REQUIRED FOR THROMBOSPONDIN AND TENASCIN MEDIATED FOCAL ADHESION DISASSEMBLY
Autore:
MURPHYULLRICH JE; PALLERO MA; BOERTH N; GREENWOOD JA; LINCOLN TM; CORNWELL TL;
Indirizzi:
UNIV ALABAMA,DEPT PATHOL,DIV MOL & CELLULAR PATHOL,G038 VOLKER HALL BIRMINGHAM AL 35294
Titolo Testata:
Journal of Cell Science
, volume: 109, anno: 1996,
parte:, 10
pagine: 2499 - 2508
SICI:
0021-9533(1996)109:<2499:CGPIRF>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
SMOOTH-MUSCLE CELLS; GROWTH FACTOR-BETA; EXTRACELLULAR-MATRIX; ENDOTHELIAL-CELLS; SIGNAL-TRANSDUCTION; MESSENGER-RNA; ALPHA-V-BETA-3 INTEGRINS; VINCULIN DISTRIBUTION; TYROSINE KINASE; EF-HAND;
Keywords:
PKG; THROMBOSPONDIN; FOCAL ADHESION; TENASCIN; SPARC;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
84
Recensione:
Indirizzi per estratti:
Citazione:
J.E. Murphyullrich et al., "CYCLIC GMP-DEPENDENT PROTEIN-KINASE IS REQUIRED FOR THROMBOSPONDIN AND TENASCIN MEDIATED FOCAL ADHESION DISASSEMBLY", Journal of Cell Science, 109, 1996, pp. 2499-2508

Abstract

Focal adhesions are specialized regions of cell membranes that are foci for the transmission of signals between the outside and the inside of the cell, Intracellular signaling events are important in the organization and stability of these structures, In previous work, we showedthat the counter-adhesive extracellular matrix proteins, thrombospondin, tenascin, and SPARC, induce the disassembly of focal adhesion plaques and we identified the active regions of these proteins, In order to determine the mechanisms whereby the anti-adhesive matrix proteins modulate cytoskeletal organization and focal adhesion integrity, we examined the role of protein kinases in mediating the loss of focal adhesions by these proteins, Data from these studies show that cGMP-dependent protein kinase is necessary to mediate focal adhesion disassembly triggered by either thrombospondin or tenascin, but not by SPARC, In experiments using various protein kinase inhibitors, we observed that selective inhibitors of cyclic GMP-dependent protein kinase, KT5823 and Rp-8-Br-cGMPS, blocked the effects of both the active sequence of thrombospondin 1 (hep I) and the alternatively - spliced segment (TNfnA-D)of tenascin-C on focal adhesion disassembly, Moreover, early passage rat aortic smooth muscle cells which have high levels of cGMP-dependent protein kinase were sensitive to hep I treatment, in contrast to passaged cGMP-dependent protein kinase deficient cells which were refractory to hep I or TNfnA-D treatment, but were sensitive to SPARC, Transfection of passaged smooth muscle cells with the catalytic domain of PKG I alpha restored responsiveness to hep I and TNfnA-D. While these studies show that cGMP-dependent protein kinase activity is necessary for thrombospondin and tenascin-mediated focal adhesion disassembly, kinase activity alone is not sufficient to induce disassembly as transfection of the catalytic domain of the kinase in the absence of additional stimuli does not result in loss of focal adhesions.

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Documento generato il 11/07/20 alle ore 13:23:23