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Table of Contents
Preface; Contents; Chapter 1: Trends in Bioprobe Research; 1.1 Introduction; 1.2 Screening of New Bioactive Compounds; 1.2.1 Cell-Based Screening; 1.2.2 Target-Based Screening; 1.3 Target Identification of Bioactive Compounds; 1.3.1 Cell Morphology-Based Profiling; 1.3.2 Proteomic Profiling; 1.3.3 Affinity Beads; 1.3.4 DARTS and CESTA; 1.4 Trends and Prospects; References; Chapter 2: Cell Proliferation and Differentiation; 2.1 Cell Growth Signaling Pathway; 2.1.1 Growth Factors and Receptors; 2.1.1.1 EGF Receptors; 2.1.1.2 Ras-MAP Kinase Pathway.
2.1.2 Cytokine Receptors Without Kinase Domains2.1.3 Cell Adhesion Receptors; 2.1.4 Dysregulation of Signaling Pathways in Cancer Cells; 2.1.4.1 Bcr-Abl Oncoprotein; 2.1.4.2 Other Abl Fusion Genes in Cancer Cells; 2.1.4.3 Inhibitor of Bcr-Abl Fusion Gene Products; 2.1.4.4 EML4-ALK Oncoprotein; 2.1.4.5 Inhibitor of EML4-ALK Fusion Gene Products; 2.1.4.6 Drug-Resistant Mutation in ALK; 2.1.4.7 Other Fusion Protein Tyrosine Kinases; 2.2 Cell Cycle Regulation; 2.2.1 Cell Cycle Regulators; 2.2.2 Cyclins and CDKs; 2.2.2.1 Cyclin and CDKs; 2.2.2.2 CDKs; 2.2.2.3 Cyclins; 2.2.2.4 CDK Inhibitors.
2.2.3 M-Phase Kinases and Their Inhibitors2.2.3.1 Plk1; 2.2.3.2 Plk1 Inhibitors; 2.2.3.3 PBD-Dependent Binding Inhibitors; 2.2.3.4 Aurora Kinases; 2.2.3.5 Aurora Kinase Inhibitors; 2.2.3.6 First-Generation Inhibitors of Aurora Kinases; 2.2.3.7 Pan-Aurora Inhibitors; 2.2.3.8 Aurora A-Specific Inhibitors; 2.2.3.9 Aurora B-Specific Inhibitors; 2.3 Cell Differentiation; 2.3.1 iPS Cells; 2.3.2 iPS Cells Induced by Small-Molecule Compounds; 2.3.3 Medical Purposes; 2.3.4 Cancer Stem Cells; 2.3.5 Small Molecules that Target CSCs; References; Chapter 3: Epigenetics; 3.1 Introduction.
3.2 Histone Acetylation3.2.1 Histone Deacetylases; 3.2.2 Histone Deacetylase Inhibitors; 3.2.2.1 Zinc-Dependent Histone Deacetylase Inhibitors; 3.2.2.1.1 Carboxylates; 3.2.2.1.2 Hydroxamic Acids; 3.2.2.1.3 Anilides; 3.2.2.1.4 Cyclic Tetrapeptides; 3.2.2.1.5 Thiols; 3.2.2.1.6 Dietary Inhibitors; 3.2.2.2 Sirtuin Inhibitors; 3.2.2.2.1 NAD Analogs; 3.2.2.2.2 Nicotinamide and Its Analogs; 3.2.2.2.3 beta-Naphthol Analogs; 3.2.2.2.4 Indoles; 3.2.2.2.5 Other Sirtuin Inhibitors; 3.2.3 Histone Acetyltransferases; 3.2.4 Histone Acetyltransferases Inhibitors; 3.2.4.1 Natural Product Inhibitors.
3.2.4.2 Bisubstrate Inhibitors3.2.4.3 C646; 3.2.5 Bromodomain and Extraterminal Protein Inhibitors; 3.3 Histone Methylation; 3.3.1 Histone Methyltransferases; 3.3.2 Lys-Specific Histone Methyltransferase Inhibitors; 3.3.2.1 G9a Inhibitors; 3.3.2.2 EZH2 Inhibitors; 3.3.2.3 Dot1L Inhibitors; 3.3.3 Histone Demethylases; 3.3.4 Lysine Demethylases Inhibitors; 3.3.4.1 Lysine Specific Demethylase 1 Inhibitors; 3.3.4.2 Jumonji Domain-Containing Histone Demethylase Inhibitors; 3.4 DNA Methylation; 3.4.1 DNA Methyltransferase Inhibitors; 3.5 Conclusions; References; Chapter 4: Apoptosis and Autophagy; 4.1 Introduction.
2.1.2 Cytokine Receptors Without Kinase Domains2.1.3 Cell Adhesion Receptors; 2.1.4 Dysregulation of Signaling Pathways in Cancer Cells; 2.1.4.1 Bcr-Abl Oncoprotein; 2.1.4.2 Other Abl Fusion Genes in Cancer Cells; 2.1.4.3 Inhibitor of Bcr-Abl Fusion Gene Products; 2.1.4.4 EML4-ALK Oncoprotein; 2.1.4.5 Inhibitor of EML4-ALK Fusion Gene Products; 2.1.4.6 Drug-Resistant Mutation in ALK; 2.1.4.7 Other Fusion Protein Tyrosine Kinases; 2.2 Cell Cycle Regulation; 2.2.1 Cell Cycle Regulators; 2.2.2 Cyclins and CDKs; 2.2.2.1 Cyclin and CDKs; 2.2.2.2 CDKs; 2.2.2.3 Cyclins; 2.2.2.4 CDK Inhibitors.
2.2.3 M-Phase Kinases and Their Inhibitors2.2.3.1 Plk1; 2.2.3.2 Plk1 Inhibitors; 2.2.3.3 PBD-Dependent Binding Inhibitors; 2.2.3.4 Aurora Kinases; 2.2.3.5 Aurora Kinase Inhibitors; 2.2.3.6 First-Generation Inhibitors of Aurora Kinases; 2.2.3.7 Pan-Aurora Inhibitors; 2.2.3.8 Aurora A-Specific Inhibitors; 2.2.3.9 Aurora B-Specific Inhibitors; 2.3 Cell Differentiation; 2.3.1 iPS Cells; 2.3.2 iPS Cells Induced by Small-Molecule Compounds; 2.3.3 Medical Purposes; 2.3.4 Cancer Stem Cells; 2.3.5 Small Molecules that Target CSCs; References; Chapter 3: Epigenetics; 3.1 Introduction.
3.2 Histone Acetylation3.2.1 Histone Deacetylases; 3.2.2 Histone Deacetylase Inhibitors; 3.2.2.1 Zinc-Dependent Histone Deacetylase Inhibitors; 3.2.2.1.1 Carboxylates; 3.2.2.1.2 Hydroxamic Acids; 3.2.2.1.3 Anilides; 3.2.2.1.4 Cyclic Tetrapeptides; 3.2.2.1.5 Thiols; 3.2.2.1.6 Dietary Inhibitors; 3.2.2.2 Sirtuin Inhibitors; 3.2.2.2.1 NAD Analogs; 3.2.2.2.2 Nicotinamide and Its Analogs; 3.2.2.2.3 beta-Naphthol Analogs; 3.2.2.2.4 Indoles; 3.2.2.2.5 Other Sirtuin Inhibitors; 3.2.3 Histone Acetyltransferases; 3.2.4 Histone Acetyltransferases Inhibitors; 3.2.4.1 Natural Product Inhibitors.
3.2.4.2 Bisubstrate Inhibitors3.2.4.3 C646; 3.2.5 Bromodomain and Extraterminal Protein Inhibitors; 3.3 Histone Methylation; 3.3.1 Histone Methyltransferases; 3.3.2 Lys-Specific Histone Methyltransferase Inhibitors; 3.3.2.1 G9a Inhibitors; 3.3.2.2 EZH2 Inhibitors; 3.3.2.3 Dot1L Inhibitors; 3.3.3 Histone Demethylases; 3.3.4 Lysine Demethylases Inhibitors; 3.3.4.1 Lysine Specific Demethylase 1 Inhibitors; 3.3.4.2 Jumonji Domain-Containing Histone Demethylase Inhibitors; 3.4 DNA Methylation; 3.4.1 DNA Methyltransferase Inhibitors; 3.5 Conclusions; References; Chapter 4: Apoptosis and Autophagy; 4.1 Introduction.