Titlebook: Cyclin Dependent Kinase (CDK) Inhibitors; Peter K. Vogt,Steven I. Reed Book 1998 The Editor(s) (if applicable) and The Author(s), under ex

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Percutaneous Access to the Urinary Tractnated manner (. et al. 1995; . and . 1995; . et al. 1996). Various mitogens, growth factors, cytokines, and a host of other agents can perturb the cell cycle machinery eliciting proliferation, differentiation, or apoptosis (. et al. 1994; . 1994). Any permanent alteration of the cell cycle-regulator

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Samuel C. Kim MD,James E. Lingeman MD, FACSng to the development of sophisticated vector systems, in combination with the establishment of mouse embryonic stem (ES) cells, targeted mutagenesis of a mouse gene is now widely used to “knock out” any gene of interest to obtain knowledge of its function. This review focuses on the approaches usin

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Kazuo Matsuda,Yasuki Kansha,Akira Kishimoto61, binding of a cyclin) and inhibitory ones (phosphorylation of T14, Y15, binding of a protein inhibitor, and ubiquitin-mediated proteolysis of the cyclin subunit). All represent potential points of intervention for the design of small-molecule inhibitors. Thus, in theory, it will be possible to id

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Cyclin Dependent Kinase (CDK) Inhibitors978-3-642-71941-7Series ISSN 0070-217X Series E-ISSN 2196-9965

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Endoscopic Imaging and Instrumentationves cells through mitosis and DNA replication. Elimination of CDK inhibitor activity, by mutation for instance, should release CDKs from this form of regulation and remove one of the restraints on cell growth.

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https://doi.org/10.1007/978-3-642-71941-7CDK; CKI; Zellzyklus; biochemistry; biology; cancer; cell; cell cycle; cellular differentiation; cellular gro