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|a Control of cell cycle and cell proliferation /
|c edited by Rossen Donev.
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|a San Diego :
|b Elsevier,
|c 2023.
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|c �2023.
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|a 1 online resource (544 pages).
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|a Advances in protein chemistry and structural biology ;
|v v. 135
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| 588 |
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|a Description based on publisher supplied metadata and other sources.
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|a Intro -- Control of Cell Cycle & -- 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.
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|a 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.
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|a 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.
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| 505 |
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|a 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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| 500 |
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|a 3.1. Cytokine-mediated HSC expansion.
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| 650 |
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|a Cell cycle
|x Regulation.
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|a Donev, Rossen.
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| 776 |
0 |
8 |
|i Print version:
|a Donev, Rossen
|t Control of Cell Cycle and Cell Proliferation
|d San Diego : Elsevier Science & Technology,c2023
|z 9780443158223
|
| 830 |
|
0 |
|a Advances in protein chemistry and structural biology ;
|v v. 135.
|
| 856 |
4 |
0 |
|u https://sciencedirect.uam.elogim.com/science/bookseries/18761623/135
|z Texto completo
|
| 880 |
8 |
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|6 505-00/(S
|a 3. Comparison between normal cells and cancerous cells -- 3.1. The dual role of p21 -- 3.2. p27kip1 -- 3.3. Pro- and anti-tumorigenic activities of p27 -- 3.4. p57kip2 -- 3.5. p16INK4a -- 3.6. p15Ink4b -- 3.7. p18Ink4c -- 3.8. p19ink4d -- 3.9. RPIC -- 4. CDKI as therapeutics -- 4.1. Pan-CDK inhibitors -- 4.2. Development of CDK selective agents -- 4.3. Drawbacks/challenges of CDKI -- 4.4. Combination therapies involving CDKI -- 5. Conclusion -- 6. Future prospects -- Acknowledgments -- Author contributions -- Conflict of interest -- Role of funding source -- References -- Chapter Six: Insights into the aberrant CDK4/6 signaling pathway as a therapeutic target in tumorigenesis -- 1. Introduction -- 2. Aberrant cell cycle checkpoints cooperate with cancer progression -- 3. AMBRA1 destabilizes cyclin D protein -- 4. Immunomodulatory function of cell cycle regulators -- 5. Cell cycle-based targeted cancer therapies -- 6. Targeting CK1ε for overcoming resistance to CDK4/6 inhibitors -- 7. Discussion -- Acknowledgment -- References -- Chapter Seven: The role of the nucleolus in regulating the cell cycle and the DNA damage response -- 1. Introduction -- 2. Nucleolus structure -- 3. The nucleolar proteome -- 4. Nucleolar assembly and disassembly during the cell cycle -- 5. The role of the nucleolus in regulating p53-dependent cell cycle events -- 6. p53-independent cell cycle regulation by nucleolar proteins -- 7. Nucleolar stress and DNA repair -- 8. The role of NPM1 in protecting from genomic instability -- 9. The nucleolus and cell death pathways -- 10. Nucleolar proteins in cancer -- 11. Conclusions -- Author contributions -- Conflicts of interest -- Acknowledgments -- References -- Chapter Eight: Chromatin regulators in DNA replication and genome stability maintenance during S-phase -- 1. Replication of chromatin.
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