[Frontiers in Bioscience 3, d887-912, August 6, 98]

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Marcos Malumbres and Angel Pellicer

Department of Pathology and Kaplan Comprehensive Cancer Center, New York University Medical Center, 550 First Avenue, New York

Received 7/17/98 Accepted 7/25/98


1. Abstract
2. Introduction
3. Ras genes and proteins
3.1. Ras families
3.2. Ras genes and proteins in mammalian cells
3.2.1. Primary structure of ras genes
3.2.2. Gene expression
3.2.3. Posttranslational modifications
3.2.4. Protein structure and biochemical function
3.3. Ras activation and transforming properties
3.4. Differences between H, K, N-ras
3.4.1. Structural differences
3.4.2. Functional differences
4. Upstream of Ras
4.1. Signal transduction from external factors to Ras
4.2. Ras activation: nucleotide exchange factors for Ras
4.2.1. Sos
4.2.2. RasGRF
4.2.3. RasGRF2
4.2.4. RasGRP
4.2.5. Some considerations on Vav, C3G and SmgGDS
4.3. Ras inactivation by GAPs
5. Downstream of Ras
5.1. Raf and the MEK/Erk pathway
5.2. RalGDS family and the Ral cascade
5.3. Phosphatidylinositol 3-kinase
5.4. Rho family: Rac, Cdc42 and Ras transformation
5.5. MEKK1 and the JNK cascade
5.6. Ras-GAPs as effectors
5.7. Other putative Ras effectors: PKC
z, AF-6, Canoe, Rin1 and Nore1
6. Ras and the cell cycle control
6.1. Cyclin D-CDK4/6 complexes and the Retinoblastoma pathway
6.2. Cyclin E-CDK2 complexes and the p27Kip1 inhibitor
6.3. Senescence response to Ras signals (p16INK4a, p15INK4b, p53 and p21Cip1)
6.4. Cooperation between oncogenes to overdrive the cell cycle
7. Perspective
7.1. Multiple pathways to control transcription, morphology and other cellular processes
7.2. Multiple pathways to control cell cycle regulation
8. Acknowledgments
9. References
9. Entire manuscript

Key words: Ras, Tumorigenesis, Signal Transduction, Cell Cycle, Cyclin-Dependent Kinases, CDK-inhibitors

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