Titlebook: Cancer Genes; Functional Aspects Enrico Mihich,David Housman Book 1996 Springer Science+Business Media New York 1996 apoptosis.cancer.cell.

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CYT

Src Family Kinases and the Cell Cycle,l similarity, including domain architecture and regulation. Topographically (from amino to carboxy terminus) they have: amino terminal acylation sites (responsible for membrane anchoring); a unique domain (40–80 amino acids that distinguish each member of the family); a Src Homology (SH) 3 domain; a

Mobile

p16 Family Inhibitors of Cyclin-Dependent Kinases,ls is their ability to enter and progress through the cell division cycle under conditions where normal cells would either be quiescent or proliferating at a reduced rate. Therefore, the molecular pathways controlling the cell division cycle must inevitably interact with pathways which regulate cell

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ASTER

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MADS-Domain Transcription Factors and their Accessory Proteins (TCFS), understanding of the regulatory mechanisms that direct gene activity of both proliferating and non-proliferating cells will provide important insight into the origin and causes of proliferative disorders in human pathology, including cancer.

步履蹒跚

Retinoblastoma Protein, Gene Expression, and Cell Cycle Control,ween quiescent and growing states. This regulation relies on the coordinated balance between inhibitory and stimulatory signals. The stimulatory factors (e.g., growth factors) and their receptors are often encoded by a class of genes called proto-oncogenes. Cells also contain several inhibitory prot

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Cyclin A-Kinase Binding to and Regulation of the Function of a Growth-Promoting Transcription Factohis role, it functions in complex with its cdk partner, cdk2 (Pines and Hunter, 1990), and it is the cyclin A-cdk2-dependent phosphorylation of selected target proteins at the appropriate time in the cell cycle which translates into the successful prosecution of its S phase function. This notwithsta