Biological Signal Transduction by Jean-Luc Galzi, Jean-Pierre Changeux (auth.), Elliott M.

By Jean-Luc Galzi, Jean-Pierre Changeux (auth.), Elliott M. Ross, Karel W. A. Wirtz (eds.)

Supplying a survey on present study in eukaryotic sign transduction, many of the themes lined are, the biochemistry and biophysics of mobilephone floor receptors, G-protein mediated signalling pathways, legislation of cyclic AMP, Ca2+, inositol phosphate pathways, the constitution and law of receptors that are tyrosine protein kinases, and mobile responses to built-in indications.

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H. (1988). Biochem. J. H. (1986). J. BioI. Chern. , Eichholtz, T. H. (1989). Cell 59, 45-54 44 Verheijden, G. H. (1990). Biochem. J. M. (1990). , and Carpenter, G. (1988). J. BioI. Chem. G. and Carpenter, G. (1990). J. BioI. Chem. 265, 3944-3948 Whiteley, B. & Glaser, L. (1986). Cell. BioI. 103, 1355-1362 Yarden, Y. & Schlessinger J. (1987). Biochemistry 26, 1434-1442 Yarden, Y. & Schlessinger J. (1987). K. Defizel, Johannes Boonstra2 , and Siegfried W. , 1984). Binding of EGF to its receptor enhances this tyrosine kinase activity, thus inducing tyrosine phosphorylation of several protein substrates including the EGF-R itself (Hunter and Cooper, 1985).

Sizes of molecular weight markers are indicated in kilodaltons. , 1990] 23 Figure 5 shows the effect of EGF on [3H]-thymidine incorporation into DNA of serumstarved, confluent cell monolayers. Control plasmid (CVN) transfected, Nlli 3T3 control cells showed no mitogenic response to EGF, yet this growth factor stimulated 3H-thymidine incorporation into all of the other transfected cell lines. However, while HERe, HER-CER, HER-CERdCT, HER-erbB-H and HER-erbB-H+CT lines were each dependent on EGF stimulation and displayed a similar dose-response profile (Figure 5A and B), HER-erbB-ES4expressing lines appeared to be EGF-independent.

1). According to the intramolecular activation model (Fig. , 1984). This model implicates that EGF-R monomers act as transmembrane signal transducers. According to the intermolecular activation model, EGF causes a shift in a hypothetical equilibrium between EGF-R monomers and dimers, resulting in enhanced tyrosine kinase activity (Fig. 1; 2). Two variations of the intermolecular activation model have been proposed. Using Triton X-lOO solubilized, purified receptor material, Das and NATO ASI Series.

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