Bioprobes : biochemical tools for investigating cell function

• Other Authors: Osada, H. 1954-
• Format: Electronic eBook
• Language: English
• Published: Tokyo : Springer, 2017.
• Edition: 2nd ed.
• Subjects: Molecular probes.; Cytology > Methodology.; elektronické knihy; electronic books
• ISBN: 9784431565291; 9784431565277
• Physical Description: 1 online resource (387 pages)

This new edition provides the most advanced research using bioprobes on the chemical control of 1) cell cycle and differentiation, 2) epigenetics, 3) apoptosis and autophagy, and 4) immune response. The "bioprobe", first proposed in the first edition, has become an indispensable tool for c...

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 Domains; 2.1.3 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 Inhibitors; 2.2.3.1 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 Acetylation; 3.2.1 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 Inhibitors; 3.2.4.3 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.