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Inhibitors of the Ras Superfamily G-proteins. Part B /
Targeted toward researchers in biochemistry, molecular and cell biology, pharmacology, and cancer, this is the second part of The Enzymes' volumes that discuss inhibitors of the Ras superfamily G-proteins. Key features: Contributions from leading authorities, Informs and updates on all the late...
| Clasificación: | Libro Electrónico |
|---|---|
| Autor principal: | |
| Otros Autores: | |
| Formato: | Electrónico eBook |
| Idioma: | Inglés |
| Publicado: |
Burlington :
Elsevier Science,
2014.
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| Colección: | Enzymes ;
v. 34. |
| Temas: | |
| Acceso en línea: | Texto completo Texto completo |
Tabla de Contenidos:
- Front Cover; Inhibitors of the Ras Superfamily G-proteins, Part B; Copyright; Contents; Preface; Chapter One: Discovery of Small-Molecule Ras Inhibitors that Display Antitumor Activity by Interfering with Ras. GTP-Effec ... ; 1. Introduction; 2. Discovery of Surface Pockets in Novel Crystal Structures of Ras. GTP; 3. Discovery of the Kobe0065-Family Compounds by In Silico Screening; 4. Inhibition of Ras Functions by the Kobe0065-Family Compounds; 4.1. Inhibition of Ras-Effector interaction; 4.2. Inhibition of proliferation of cultured cancer cells.
- 4.3. Inhibition of tumor growth in a xenograft model5. Structural Basis for Inhibition of Ras Functions by the Kobe0065-Family Compounds; 6. Specificity of the Kobe0065-Family Compounds Toward Various Small GTPases; 7. Discussion and Conclusion; Acknowledgments; References; Chapter Two: An Orthosteric Inhibitor of the RAS-SOS Interaction; 1. Introduction; 2. RAS Signaling in Normal Physiology and Malignancy; 3. Strategies for Targeting RAS Activity; 4. Inhibitor Design; 5. RAS Binding; 6. Cell Entry and Intracellular Effects; 7. Conclusions; References.
- Chapter Three: Conformation-Specific Inhibitors of Raf Kinases1. Introduction; 2. Kinase Conformations and Different Types of Kinase Inhibitors; 3. Representative Raf Inhibitors and Their Binding Modes; 4. Raf Kinase Dimerization and Activation; 5. Perspective; 6. Conclusion; Acknowledgments; References; Chapter Four: Inhibitors of the ERK Mitogen-Activated Protein Kinase Cascade for Targeting RAS Mutant Cancers; 1. Introduction; 2. Ras and the ERK MAPK Effector Signaling Network; 2.1. H-Ras, K-Ras4A/4B, and N-Ras; 2.2. A-Raf, B-Raf, and C-Raf/Raf-1; 2.3. MEK1 and MEK2; 2.4. ERK1 and ERK2.
- 3. Role of the ERK MAPK Cascade in Mutant RAS-Dependent Tumor Progression and Maintenance4. MEK1/2 Inhibitors; 4.1. Trametinib; 4.2. Selumetinib; 4.3. Pimasertib; 4.4. Cobimetinib; 4.5. PD0325901; 4.6. Refametinib; 4.7. AZD8330; 4.8. TAK-733; 4.9. MEK162; 4.10. RO5126766; 4.11. RO4987655; 4.12. E6201; 5. ERK1/2 Inhibitors; 5.1. SCH772984; 5.2. MK-8353/SCH900353; 5.3. BVD-523; 5.4. VTX11e; 5.5. AEZS-131/AEZS-134; 5.6. FR180204; 6. Issues and Questions; Acknowledgments; References; Chapter Five: Inhibiting the RAS-PI3K Pathway in Cancer Therapy; 1. Introduction; 2. The PI3K Pathway.
- 3. PI3K Inhibitors4. PI3K Pathway Inhibitors; 5. Inhibiting PI3K in Cancer; 6. Future Directions; References; Chapter Six: The RalGEF/Ral Pathway: Evaluating an Intervention Opportunity for Ras Cancers; 1. Introduction; 1.1. Oncogenic Ras signaling: Targeting troubles prompt alternative approaches; 1.2. RalGEF/Ral pathway overview; 1.2.1. RalGEFs; 1.2.2. Ral GTPases and their effectors; 1.2.3. RalGAPs; 2. RalGEF/Ral Signaling and Cancer: A Rationale for Pathway Inhibition; 2.1. Evidence from tumor cell models; 2.2. Evidence from genetically engineered mouse models.