Control of cell cycle and cell proliferation /

Detalles Bibliográficos
Clasificación:Libro Electrónico
Otros Autores: Donev, Rossen
Formato: Electrónico eBook
Idioma:Inglés
Publicado: San Diego : Elsevier, 2023.
Colección:Advances in protein chemistry and structural biology ; v. 135.
Temas:
Cell cycle > Regulation.
Cell proliferation.
Cycle cellulaire > R�egulation.
Cellules > Prolif�eration.
Acceso en línea:Texto completo
Tabla de Contenidos:
  • Intro
  • Control of Cell Cycle &amp
  • Cell Proliferation
  • Copyright
  • Contents
  • Contributors
  • Chapter One: Exploiting pivotal mechanisms behind the senescence-like cell cycle arrest in cancer
  • 1. Introduction
  • 2. Senescence-like cell cycle arrest in cancer
  • 3. General signaling pathways engaged in senescence-like cell cycle arrest
  • 3.1. p53/p21-dependent apoptotic pathways: Passing through caspases and apoptotic proteins
  • 3.2. p16INK4A/pRB pathway
  • 3.3. CDK/cyclin complexes
  • 3.4. DREAM complex
  • 4. Conclusion
  • 5. Future perspective
  • Acknowledgment
  • Author contributions
  • Conflict of interest statement
  • References
  • Chapter Two: Cyclin-dependent kinases in cancer: Role, regulation, and therapeutic targeting
  • 1. Introduction
  • 2. Cyclins and cyclin-dependent kinases in cell cycle progression
  • 2.1. Early G1 phase and CDK/cyclin complexes
  • 2.2. Regulation of cyclin D/E kinase activity by CDKs
  • 2.3. Regulation of G1 progression via cyclin E
  • 2.4. Control of DNA synthesis via cyclin A
  • 2.5. Control of mitosis via cyclin B/cyclin-dependent kinase 1 (CDK1)
  • 2.6. Spindle assembly checkpoint
  • 2.7. Anaphase
  • 2.8. Cytokinesis
  • 3. Cyclin-dependent kinase inhibitors (CDKIs) in cancer therapeutics
  • 3.1. First generation pan CDK inhibitors
  • 3.2. Second-generation pan CDK inhibitors
  • 3.3. Selective CDK inhibitors
  • 3.3.1. CDK1 inhibitor
  • 3.3.2. CDK4/6 inhibitor
  • 3.3.3. CDK7 inhibitors
  • 3.3.4. CDK9 inhibitors
  • 3.3.5. CDK8/19 inhibitors
  • 4. Conclusion
  • Acknowledgments
  • Declarations
  • Ethical approval and consent to participate
  • Consent for publication
  • Availability of supporting data
  • Competing interests
  • References
  • Chapter Three: Computational screening and structural analysis of Gly201Arg and Gly201Asp missense mutations in human cyc ...
  • 1. Introduction.
  • 2. Materials and methods
  • 2.1. Retrieval of mutations from COSMIC
  • 2.2. Screening of mutations using computational algorithm
  • 2.3. Comparative computational simulations of native and CDK4 mutants
  • 3. Results and discussion
  • 3.1. Cyclin-dependent kinase 4 (CDK4) and cancers
  • 3.2. Retrieval of mutations from cosmic database
  • 3.3. Screening of mutations using computational algorithm
  • 3.3.1. Screening of CDK4 missense mutations inducing pathogenicity
  • 3.3.2. Screening of CDK4 missense mutations inducing stability changes in protein
  • 3.3.3. Predicting the most significant mutations altering the protein structure
  • 4. Conclusion
  • Acknowledgment
  • Conflict of interest
  • Author contributions
  • Funding
  • References
  • Chapter Four: Controlling cell proliferation by targeting cyclin-dependent kinase 6 using drug repurposing approach
  • 1. Introduction
  • 2. Methodology
  • 2.1. Protein data acquisition
  • 2.2. Binding site identification
  • 2.3. Compound retrieval
  • 2.4. Structure-based virtual screening
  • 2.5. ADME
  • 2.6. Toxicity (Mcule)
  • 2.7. Docking
  • 2.8. Molecular dynamics simulation
  • 2.9. Essential dynamics
  • 3. Results
  • 3.1. Protein data acquisition
  • 3.2. Binding site identification
  • 3.3. Compound retrieval
  • 3.4. Virtual screening
  • 3.5. ADME and toxicity analysis
  • 3.6. Molecular docking
  • 3.7. Molecular dynamics simulation and analysis
  • 4. Discussion
  • 5. Conclusion
  • Acknowledgments
  • Conflict of interest
  • Author contributions
  • Funding
  • References
  • Chapter Five: CDK regulators-Cell cycle progression or apoptosis-Scenarios in normal cells and cancerous cells
  • 1. Introduction
  • 2. CDK regulators
  • 2.1. CDK activating kinases
  • 2.2. CDK regulatory subunit
  • 2.3. Regulatory inhibitory phosphorylation
  • 2.4. CDK inhibitory proteins
  • 2.5. miRNA.
  • 2. Cellular response to replication stress
  • 3. Chromatin factors involved in DNA replication initiation
  • 4. Chromatin in the maintenance of DNA replication elongation and replication stress protection
  • 5. Chromatin events at stalled forks
  • 6. Transcription-induced replication stress
  • 7. Exploiting replication stress
  • 8. Concluding remarks
  • Acknowledgments
  • References
  • Chapter Nine: Role of macrophages in cancer progression and targeted immunotherapies
  • 1. Overview of tumor-associated macrophages
  • 2. Polarization of TAMs
  • 3. TAMs involvement in tumor progression
  • 3.1. Cellular plasticity
  • 3.2. Heterogeneity
  • 3.3. Angiogenesis
  • 3.4. Metastasis
  • 4. Role of TAMs in immune response
  • 4.1. Immunosuppression
  • 4.2. Chemoresistance
  • 5. Cell cycle regulation in TAMs and cancer cells
  • 5.1. Role of cyclin-dependent kinases in TAM differentiation
  • 5.2. TAM-dependent cancer cell cycle progression
  • 5.3. TAM-induced cancer cell senescence
  • 6. Therapies targeting cancer cell cycle progression by targeting TAMs
  • 6.1. Cell cycle inhibitors targeting TAM differentiation and tumor progression
  • 6.2. CAR macrophage immunotherapy
  • 7. Future directions
  • References
  • Chapter Ten: Therapeutic targets in cancer treatment: Cell cycle proteins
  • 1. Introduction
  • 2. Tumor cell cycle phase analysis
  • 3. Cell-cycle checkpoint
  • 4. Targeting cell cycle kinases in cancer therapy
  • 5. Role of D-type cyclins in cancer
  • 6. Role of cyclin E in cancer
  • 7. Role of cyclin B and CDK1 in cancer
  • 8. Role of polo-like kinases (Plks) family members in cancer
  • 9. Plks in cancer development
  • 10. DNA damage checkpoint kinases
  • 10.1. Targeting mutated p53
  • 10.2. Aurora kinase signaling
  • 10.3. BRCA1/2
  • 10.4. Wingless (WNT) signaling
  • 11. Currently used cyclin inhibitors
  • 12. Concluding remarks
  • Acknowledgments.
  • Declaration: Conflict of interest
  • References
  • Chapter Eleven: Anti-cancer drug molecules targeting cancer cell cycle and proliferation
  • 1. Introduction
  • 2. Overview of cell cycle checkpoints
  • 3. Disturbance in cancer cell cycle checkpoints
  • 4. Anti-cancer drugs
  • 4.1. Historical perspective of anti-cancer drugs
  • 4.2. Modern phase of anti-cancer drug development
  • 5. Drugs that target cell cycle proteins
  • 5.1. Targeting G1 phase regulatory proteins
  • 5.2. S-phase targeted therapeutics
  • 5.3. G2 and M phase inhibitors
  • 5.4. Inhibitors of WEE1 and CHK1 kinases
  • 5.5. Aurora kinase and polo kinase inhibitors
  • 6. Cancer cell proliferation inhibitors
  • 6.1. Hormone, hormone receptors, and cancer cell proliferation
  • 7. Conclusion
  • References
  • Chapter Twelve: Cellular signals integrate cell cycle and metabolic control in cancer
  • 1. Growth factors in cancer
  • 2. Growth factor signal transduction and biological responses
  • 3. Growth factor-dependent signaling and cell cycle progression
  • 4. The cell cycle controls the metabolism
  • 4.1. Cyclins and their kinases modulate metabolism during each phase of cell cycle
  • 4.2. p53 tumor suppressor protein monitors metabolic imbalance at cell cycle checkpoints
  • 4.3. Failure to maintain metabolism during the cell cycle triggers apoptosis
  • 5. Conclusion
  • References
  • Chapter Thirteen: Therapeutic targeting and HSC proliferation by small molecules and biologicals
  • 1. Introduction
  • 1.1. The apple of regenerative medicine�s eyes: Hematopoietic stem cells
  • 1.2. Characterization of hematopoietic stem cells
  • 1.3. The niche of hematopoietic stem cells
  • 1.4. Metabolism of hematopoietic stem cells
  • 2. Cell cycle kinetics of hematopoietic stem cells
  • 2.1. Cell intrinsic factors
  • 2.2. Cell extrinsic factors
  • 3. Hematopoietic stem cells expansion technologies.

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