August Biological Response Mediators and Modulators

John Jacob Abel Symposia on Drug Development
1. Auflage 2013
ISBN: 978-1-4832-1625-6
Verlag: Elsevier Science & Techn.
Format: PDF
Kopierschutz: 1 - PDF Watermark

E-Book, Englisch, 274 Seiten, Web PDF

Biological Response Mediators and Modulators explains that the behavior of a cell depends upon the absorption of the ligand, the quantity of functional receptors existing for ligand recognition and binding, and the transduction of the signal through successive intercellular events. The book presents such model systems as the low-density lipoprotein (LDL) receptor, the epidermal growth factor receptor, and the insulin receptor. The LDL receptor is a model for a class of surface receptors that facilitate the cellular application of macromolecules through the process of receptor-mediated endocytosis. The book discusses the general characteristics of receptor-mediated endocytosis. Another topic of interest is the property of growth-related cell surface receptors. The section that follows describes the function of these receptors as tyrosine-specific protein kinases, which is related to the protein yields of some viral oncogenes. The amount of receptors in a cell depends upon the rates of synthesis and inactivation. The book will provide valuable insights for scientists, cytologists, students, and researchers in the field of chemistry.

Autoren/Hrsg.

August, J. Thomas

Inhaltsverzeichnis

1;Front Cover;1
2;Biological Response Mediators and Modulators;4
3;Copyright Page;5
4;Table of Contents;8
5;Contributors;12
6;Preface;16
7;Acknowledgments;20
8;CHAPTER 1. RECEPTOR-MEDIATED ENDOCYTOSIS AS EXEMPLIFIED BY THE LOW DENSITY LIPOPROTEIN RECEPTOR;22
8.1;General Characteristics of Receptor-Mediated Endocytosis;22
8.2;Pathway of Receptor-Mediated Endocytosis: The LDL Receptor;24
8.3;Mechanism by Which LDL Receptors Reach Coated Pits;25
8.4;Recycling of the LDL Receptor;26
8.5;Functional Domains of the LDL Receptor: Biosynthesis Studies;26
8.6;References;27
9;CHAPTER 2. THE RECEPTOR FOR EGF FUNCTIONS AS A TYROSINE-SPECIFIC PROTEIN KINASE;28
9.1;References;32
10;CHAPTER 3. REGULATION OF INSULIN RECEPTOR METABOLISM: MECHANISM OF INSULIN-INDUCED RECEPTOR DOWN-REGULATION;34
10.1;Change in Insulin Receptor Level Induced by Insulin;35
10.2;Synthetic and Degradative Rates of Insulin Receptor in Control and Down-regulated Cells;38
10.3;Effect of Insulin-Induced Down-Regulation on Insulin-Stimulated [1-14C]12-Deoxyglucose Transport;44
10.4;Characterization of Cell Surface Insulin Receptor Cross-linked Covalently to 1 2 5I-Insulin;44
10.5;Rate of Appearance of Heavy Receptors at and Loss of Light Receptors from the Plasma Membrane Following the Shift of Cells to Heavy Amino Acids;47
10.6;Effect of Insulin on the Rates of Appearance of Newly-Synthesized Receptor at and the Net Removal of Previously-Synthesized Receptors from the Cell Surface;50
10.7;Discussion;54
10.8;Acknowledgments;58
10.9;References;59
11;CHAPTER 4. METABOLISM OF ARACHIDONIC ACID BY THE CYCLOOXYGENASE PATHWAY IN MAST CELLS AND BY THE 15- LIPOXYGENASE PATHWAY IN HUMAN EOSINOPHILS;62
11.1;Acknowledgments;68
11.2;References;68
12;CHAPTER 5. PHYSIOLOGIC AND PATHOBIOLOGIC EFFECTS OF LEUKOTRIENES C4, D4, AND E4;70
12.1;Arachidonic Acid Metabolism in the 5-lipoxygenase Pathway;70
12.2;Biological Effects on the Leukotrienes;71
12.3;Cell Sources of the Leukotrienes;74
12.4;Acknowledgment;75
12.5;References;75
13;CHAPTER 6. BIOLOGICAL ACTVITIES OF LEUKOTRIENE B4 AND OTHER HYDROXYEICOSATETRAENOIC ACIDS (HETEs);80
13.1;Formation of Leukotriene B* and Other Hydroxyeicosatetraenoic Acids;80
13.2;Biological Activities of Leukotriene B4 and Other Hydroxyeicosatetraenoic Acids;81
13.3;Conclusions;85
13.4;References;86
14;CHAPTER 7. ACETYL GLYCERYL ETHER PHOSPHORYLCHOLINE (AGEPC) A MODEL ANAPHYLACTOMIMETIC MEDIATOR;88
14.1;Anaphylactomimetic Mediators;88
14.2;Vasoactive Activity of AGEPC;91
14.3;Smooth Muscle Contracting Activities of AGEPC;92
14.4;AGEPC-induced Systemic Anaphylactoid Reactions;93
14.5;Concluding Remarks;98
14.6;Acknowledgments;100
14.7;References;102
15;CHAPTER 8. THE ROLE OF LIPOXYGENASE PRODUCTS OF ARACHIDONIC ACID IN INFLAMMATORY EVENTS MEDIATED BY HUMAN BASOPHILS AND MAST CELLS;104
15.1;Methods and Results;105
15.2;The Effect of Lipoxygenase Products on Histamine Release from Human Basophils and Mast Cells;105
15.3;The Modulation of Histamine Release from Human Basophils and Mast Cells;111
15.4;Discussion;114
15.5;Acknowledgments;116
15.6;References;116
16;CHAPTER 9. THE CHEMISTRY AND BIOLOGY OF C3a, C4a, AND C5a AND THEIR EFFECTS ON CELLS;120
16.1;Correlations Between Anaphylatoxin Structure and Function;122
16.2;A Duality of Anaphylatoxin Action on Pulmonary Tissue;125
16.3;Duality of the Action of Anaphylatoxinsin Immunoregulation;132
16.4;Summary and Conclusion;136
16.5;Acknowledgments;136
16.6;References;136
17;CHAPTER 10. ON THE SIZE HETEROGENEITY AND MOLECULAR COMPOSITION OF THE TRANS-MEMBRANE CHANNELS PRODUCED BY COMPLEMENT;138
17.1;Initial Indication from Electrical Conductance Experiments that Complement Channels are Heterogeneous with Respect to Size;140
17.2;Molecular Sieving Estimates of the Maximal Size of C5b-8 and C5b-9 Channels;141
17.3;Studies of the Heterogeneity of C5b-9 Channels by Molecular Sieving with Paired Markers;145
17.4;The Relation Between Channel Size and the Molecular Composition of the C5b-9 Complex;146
17.5;Functional Analysis of the Number of C5b6, C7, C8, and C9 Molecules Required for a Single Channel;148
17.6;Disappearance of Small Channels at High C9 Multiplicity;152
17.7;Models of Channel Structure;155
17.8;Summary;158
17.9;Acknowledgments;158
17.10;References;159
18;CHAPTER 11. MEMBRANE DAMAGE BY COMPLEMENT COMPONENTS C5b-C9: BIOCHEMICAL AND ULTRASTRUCTURAL STUDIES;162
18.1;Nomenclature;164
18.2;Properties of Fluid-phase Terminal Complement Complexes;164
18.3;Subunit Composition;165
18.4;Amphiphilic Properties;168
18.5;Molecular Weight;171
18.6;Ultrastructure and Membrane Orientation;173
18.7;Is the Unit Complement Lesion a C5b~9 Monomer or Dimer?;176
18.8;Mechanism of Membrane Damage by C5b-9(m);177
18.9;Perspectives;180
18.10;Acknowledgments;181
18.11;References;181
19;CHSPTER 12. CYTOKINE-CELL INTERACTIONS THAT MODULATE INFLAMMATORY REACTIONS;184
19.1;Interleukin 1 (IL-1);186
19.2;Colony Stimulating Factors;192
19.3;Interleukin 2 (IL-2);192
19.4;Interferon;193
19.5;Sequential Cytokine-Cell Interactions;193
19.6;Immunopharmacological Implications;194
19.7;References;196
20;CHAPTER 13. INTERLEUKIN-2 AND THE REGULATION OF CYTOTOXIC CELLS;198
20.1;Results;199
20.2;Discussion;202
20.3;References;203
21;CHAPTER 14. PHARMACOLOGICAL MODULATIONS OF IgE-BINDING FACTOR;206
21.1;Formation of IgE-potentiating Factors and IgE-suppressive Factors by Lymph Node Cells of Rats Infected with Nippostrongylus brasiliensis;206
21.2;Pharmacologie Modulation of IgE-binding Factors;209
21.3;Participation of Lipomodulin in the Selective Formation of IgE-suppressive Factors by Complete Freund's Adjuvant Treatment;212
21.4;Summary;216
21.5;Acknowledgments;217
21.6;References;217
22;CHAPTER 15. MECHANISMS OF ANTIVIRAL ACTION OF INTERFERONS;220
22.1;Antiviral Actions of Interferons;221
22.2;Sensitivity of Various Cell Lines to Interferon;225
22.3;DNA Viruses and Interferons;226
22.4;Interferon-induced Enzymes and Cell Growth;227
22.5;Summary;227
22.6;References;228
23;CHAPTER 16. PHARMACOLOGICAL MANIPULATION OF THE CHEMOTACTIC FACTOR RECEPTOR ON LEUKOCYTES;232
23.1;Summary;239
23.2;References;240
24;CHAPTER 17. SECRETORY PRODUCTS IN CYTOTOXICITY;242
25;T Cells;244
25.1;NK Cells and K Cells;248
25.2;Granulocytes;249
25.3;Macrophages;249
25.4;Conclusions;255
25.5;Acknowledgments;257
25.6;References;257
26;CHAPTER 18. ANTIBODY-MEDIATED TUMOR SUPPRESSION: POSSIBLE ROLE OF LYSOPHOSPHATIDYLCHOLINE AND INTERLEUKIN;262
26.1;Lysophosphatidylcholine;264
26.2;Interleukin;267
26.3;Concluding Remarks;269
26.4;Acknowledgments;270
26.5;References;270
27;Index;272