Books+ Search Results
Control of Cell Cycle and Cell Proliferation
Author
Title
Control of Cell Cycle and Cell Proliferation.
ISBN
9780443158223
0443158223
9780443158230
0443158231
Publication
San Diego : Elsevier Science & Technology, 2023.
Copyright Notice Date
©2023
Physical Description
1 online resource (544 pages).
Local Notes
Access is available to the Yale community.
Notes
3.1. Cytokine-mediated HSC expansion.
Description based on publisher supplied metadata and other sources.
Access and use
Access restricted by licensing agreement.
Variant and related titles
Elsevier ScienceDirect All Books. OCLC KB.
Other formats
Print version: Donev, Rossen Control of Cell Cycle and Cell Proliferation San Diego : Elsevier Science & Technology,c2023
Format
Books / Online
Language
English
Added to Catalog
June 06, 2023
Series
Issn Series
Contents
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.
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.
Genre/Form
Electronic books.
Also listed under
Bookmark As
Citation
