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Viral Cytopathology: Cellular Macromolecular Synthesis and Cytocidal Viruses Including a Cumulative Index to the Authors and Major Topics C

ISBN-13: 9781461357025 / Angielski / Miękka / 2012 / 556 str.

Heinz Fraenkel-Conrat; Robert R. Wagner
Viral Cytopathology: Cellular Macromolecular Synthesis and Cytocidal Viruses Including a Cumulative Index to the Authors and Major Topics C Fraenkel-Conrat, Heinz 9781461357025 Springer - książkaWidoczna okładka, to zdjęcie poglądowe, a rzeczywista szata graficzna może różnić się od prezentowanej.

Viral Cytopathology: Cellular Macromolecular Synthesis and Cytocidal Viruses Including a Cumulative Index to the Authors and Major Topics C

ISBN-13: 9781461357025 / Angielski / Miękka / 2012 / 556 str.

Heinz Fraenkel-Conrat; Robert R. Wagner
cena 200,77
(netto: 191,21 VAT:  5%)

Najniższa cena z 30 dni: 192,74
Termin realizacji zamówienia:
ok. 22 dni roboczych
Dostawa w 2026 r.

Darmowa dostawa!

The time seems ripe for a critical compendium of that segment of the biological universe we call viruses. Virology, as a science, having passed only recently through its descriptive phase of naming and numbering, has probably reached that stage at which relatively few new-truly new-viruses will be discovered. Triggered by the intellectual probes and techniques of molecular biology, genetics, bio- chemical cytology, and high resolution microscopy and spectroscopy, the field has experienced a genuine information explosion. Few serious attempts have been made to chronicle these events. This comprehensive series, which will comprise some 6000 pages in a total of 19 volumes, represents a commitment by a large group of active investigators to analyze, digest, and expostulate on the great mass of data relating to viruses, much of which is now amorphous and disjointed, and scattered throughout a wide literature. In this way, we hope to place the entire field in perspective, and to develop an invaluable reference and sourcebook for researchers and students at all levels. This series is designed as a continuum that can be entered any- where, but which also provides a logical progression of developing facts and integrated concepts.

Kategorie:
Nauka, Medycyna
Kategorie BISAC:
Gardening > General
Medical > Microbiology
Science > Botanika
Wydawca:
Springer
Seria wydawnicza:
Comprehensive Cytopathology
Język:
Angielski
ISBN-13:
9781461357025
Rok wydania:
2012
Wydanie:
1984
Numer serii:
000297383
Ilość stron:
556
Waga:
1.05 kg
Wymiary:
25.4 x 17.8
Oprawa:
Miękka
Wolumenów:
01

1 Cytopathic Effects of Viruses: A General Survey.- 1. Defining the Problem.- 2. Historical Background.- 2.1. Early Observations on Virus-Induced Cytopathology.- 2.2. Early Observations on Virus-Induced Alterations in Cell Macromolecular Synthesis.- 3. Viral Cytopathology: General Principles.- 3.1. Cellular Differentiation and Susceptibility to Viral Infection.- 3.2. Methods for Studying Viral Cytopathic Effects.- 3.3. Variability of Cytopathic Effects.- 4. Specific Cytopathic Viruses: An Overview.- 4.1. Picornavirus Cytopathology.- 4.2. Poxvirus Cytopathology.- 4.3. Rhabdovirus Cytopathology.- 4.4. Adenovirus Cytopathology.- 4.5. Viral Toxicity.- 5. Some Subcellular Targets of Pathogenic Viruses.- 5.1. Cellular Membrane Effects of Certain Viruses.- 5.2. Effects of Viruses on Lysosomes.- 5.3. Effects of Viruses on the Cytoskeleton.- 6. Summary.- 7. References.- 2 Transcription by RNA Polymerase II.- 1. Introduction.- 2. Polymerase II Control Regions: In Vivo.- 2.1. Initiation Regions.- 2.2. Immediate Upstream Sequences.- 2.3. Enhancer Regions.- 3. Polymerase II Promoters: In Vitro.- 3.1. Initiation Region.- 3.2. Immediate Upstream Region.- 3.3. Enhancer Region.- 4. RNA Polymerase II and Factors.- 4.1. RNA Polymerase II.- 4.2. Termination of Transcription.- 4.3. Factors Necessary for Accurate Transcription.- 4.4. Promoter-Specific Factors.- 5. Closing Comments.- 6. References.- 3 Regulation of Eukaryotic Translation.- 1. Introduction.- 2. The Rate-Limiting Step in Translation.- 3. Functional Domains in Messenger RNA.- 3.1. AUG Initiation Codon.- 3.2. The 5?-Terminal Cap Structure.- 3.3. 5?-Leader Sequence.- 3.4. 3?-Terminal Poly (A).- 3.5. 3?-Untranslated Sequence.- 4. Initiation of Translation.- 4.1. Dissociation of Ribosomes into Subunits.- 4.2. Recognition of Met-tRNAf by eIF-2.- 4.3. Binding of Met-tRNAf/eIF-2/GTP to 40 S Subunits.- 4.4. The mRNA-Binding Step.- 5. Role of Initiation Factors in Binding of mRNA.- 5.1. Initiation Factor 2.- 5.2. Other Initiation Factors.- 6. Translational Control by mRNA Competition.- 6.1. mRNA Competition for eIF-2.- 6.2. mRNA Competition for Other Initiation Factors.- 6.3. Further Examples of mRNA Competition.- 7. Translational Control by Regulation of eIF-2 Activity.- 7.1. Heme Deprivation.- 7.2. Double-Stranded RNA.- 7.3. Interferon.- 7.4. Other Conditions that Affect eIF-2 Activity.- 7.5. Nature of the Translational Inhibitor.- 8. Translational Regulation by Other Means.- 8.1. Translational Repression.- 8.2. Heat Shock.- 8.3. Phosphorylation of Ribosomal Protein.- 8.4. Virus-Induced Shut-Off of Host Translation.- 9. Parameters Determining Translational Efficiency of an mRNA Species.- 10. References.- 4 Picornavirus Inhibition of Host Cell Protein Synthesis.- 1. Introduction and Scope.- 2. Properties of Inhibition of Host Cell Protein Synthesis by Poliovirus.- 2.1. General Description.- 2.2. Requirement for Expression of Viral Genome.- 2.3. Poliovirus Inhibition of Other Viral Protein Synthesis.- 2.4. Integrity of Untranslated mRNA.- 3. Proposed Models for Inhibition.- 3.1. Double-Stranded RNA.- 3.2. Viral Capsid Proteins.- 3.3. Inherent Translational Efficiencies.- 3.4. Membrane Alterations and Intracellular Ionic Modifications.- 3.5. Inactivation of Initiation Factors.- 4. Initiation Factors.- 4.1. Summary of Eukaryotic Initiation Factors.- 4.2. Involvement of Initiation Factors in Poliovirus-Induced Inhibition of Cellular Protein Synthesis: Discovery of Cap-Binding Protein.- 5. Cap Recognition Activity.- 5.1. The 24,000-Dalton Cap-Binding Protein.- 5.2. ATP/Mg2+-Dependent Cap-Binding Proteins.- 5.3. Cap-Binding Protein Complex: eIF-4F.- 5.4. Cap-Binding Proteins in Poliovirus-Infected Cells.- 5.5. Function of Cap-Binding Proteins.- 6. Polioviral Mediator of Host Cell Shut-off.- 7. Other Picornaviruses.- 7.1. Differences from Poliovirus.- 7.2. mRNA Competition.- 7.3. Host Cell-Specific Interactions.- 7.4. Role of Alterations in Ionic Environment.- 7.5. Unstudied Picornaviruses.- 8. Other Viruses That May Utilize Mechanisms Similar to Poliovirus.- 8.1. Reovirus.- 8.2. Semliki Forest Virus.- 8.3. Frog Virus 3.- 9. Concluding Remarks.- 10. References.- 5 Rhabdovirus Cytopathology: Effects on Cellular Macromolecular Synthesis.- 1. Introduction.- 2. Properties of Rhabdoviruses: A Brief Survey.- 2.1. Structure—Function Relationships.- 2.2. Reproduction Strategies of Rhabdoviruses.- 2.3. Rhabdovirus Genetics.- 3. Cellular Responses to Rhabdovirus Infection.- 3.1. Cytopathology.- 3.2. Variations in Host Cell Susceptibility.- 4. Protein Synthesis Inhibition by Vesicular Stomatitis Virus.- 4.1. Definition of the Problem.- 4.2. Host Cell and Environmental Factors.- 4.3. Viral Properties as Candidates for Inhibiting Cell Protein Synthesis.- 4.4. VSV Genetics and Protein Synthesis Inhibition.- 4.5. Inhibitors of VSV Functions that Affect Protein Synthesis Inhibition.- 4.6. Competition between Cell and Viral Messengers?.- 4.7. Viral Products as Putative Inhibitors of Cellular Protein Synthesis.- 4.8. Cellular Target for Inhibition of Protein Synthesis.- 5. VSV Inhibition of Cellular Nucleic Acid Synthesis.- 5.1. Host Cell Responses.- 5.2. Viral Properties as Candidates for Inhibiting Cellular Nucleic Acid Synthesis.- 5.3. Temperature-Sensitive Mutants and DI Particles Restricted in Transcription.- 5.4. Use of UV Irradiation to Identify VSV Genetic Information Responsible for Shutting Off Cellular RNA Synthesis.- 5.5. Cellular Targets for VSV Inhibition of RNA Synthesis.- 5.6. Inhibition of Transcription Initiation on DNA Templates in Cell-Free Systems.- 5.7. Effect of VSV on Cellular and Viral DNA Synthesis.- 6. Summary.- 7. References.- 6 Adenovirus Cytopathology.- 1. Introduction.- 2. Adenovirus—Mammalian Cell Interactions.- 2.1. The Adenovirus Productive Cycle.- 2.2. Abortive and Partially-Productive Infections.- 2.3. General Features of the Response of Permissive Cells to Adenovirus Infection.- 3. Effects of Adenovirus Infection on Cellular DNA Metabolism.- 3.1. Inhibition of Cellular DNA Synthesis in Productively-Infected Cells.- 3.2. The Induction of Cellular DNA Synthesis in Quiescent Cells.- 4. Cellular RNA Metabolism in Adenovirus-Infected Cells.- 4.1. Inhibition of Production of Cellular mRNA.- 4.2. Induction of Cellular Gene Expression in Adenovirus-Infected Cells.- 4.3. Posttranscriptional and Transcriptional Regulation of Ribosomal RNA Synthesis in Adenovirus-Infected Cells.- 5. Selective Translation of Viral mRNA in Productively-Infected Cells.- 6. Summary and Conclusions.- 7. References.- 7 The Effects of Herpesviruses on Cellular Macromolecular Synthesis.- 1. Introduction.- 2. Early Studies.- 3. Effects on DNA Synthesis.- 4. Effects on RNA Synthesis.- 4.1. General.- 4.2. Messenger RNA.- 4.3. Functional mRNA.- 5. Effects on Protein Synthesis.- 5.1. Polyribosomes.- 5.2. Polypeptides.- 5.3. Enzymes.- 5.4. A Virion-Associated Inhibitor.- 5.5. Two Distinct Stages.- 5.6. Specificity of Shut-off.- 5.7. Cellular Stress Proteins.- 5.8. Differences between HSV-1 and HSV-2.- 5.9. Genetic Mapping.- 6. Other Herpesviruses.- 6.1. Epstein—Barr Virus.- 6.2. Herpesvirus Saimiri.- 6.3. Cytomegalovirus.- 7. Mechanisms.- 7.1. Multiplicity of Infection.- 7.2. Breakdown of Polysomes.- 7.3. Reversibility of Early Shut-off.- 7.4. Ionic Imbalance.- 7.5. Delayed Shut-off.- 7.6. Inhibition of Transcription.- 7.7. Inhibition of DNA Synthesis.- 7.8. Relationship between DNA and Protein Shut-off.- 7.9. Inhibition of ?-Protein Synthesis.- 8. Conclusion.- 9. References.- 8 Poxvirus Cytopathogenicity: Effects on Cellular Macromolecular Synthesis.- 1. Introduction.- 1.1. Virus Cytopathogenicity.- 1.2. Poxvirus Structure.- 1.3. Poxvirus Replication.- 2. Poxvirus Cytopathogenicity.- 2.1. Mechanisms of Morphological Lesions.- 2.2. Inhibition of Host Cell RNA Synthesis.- 2.3. Inhibition of Host Cell DNA Synthesis.- 2.4. Inhibition of Host Protein Synthesis.- 3. Concluding Remarks.- 4. References.- 9 Reovirus Cytopathology: Effects on Cellular Macromolecular Synthesis and the Cytoskeleton.- 1. Introduction.- 1.1. Reovirus Structure.- 1.2. The Reovirus Replicative Cycle.- 1.3. Reovirus Genetics and the Genetic Approach to the Analysis of Reovirus Cytopathogenicity.- 2. Reovirus Effects on Host Cell DNA Synthesis.- 3. Reovirus Effects on Host Cell RNA and Protein Synthesis.- 4. Reovirus Effects on Cytoskeletal Organization.- 5. Summary.- 6. References.- 10 Inhibition of Host Cell Macromolecular Synthesis following Togavirus Infection.- 1. Introduction.- 2. Acute Infection by Alphaviruses in Vertebrate Cell Cultures.- 2.1. Effect on Cellular Protein Synthesis.- 2.2. Effect on Cellular RNA Synthesis.- 2.3. Effect on Cellular DNA Synthesis.- 2.4. Necessary Host Components for Viral Replication.- 3. Chronic and Persistent Infection by Alphaviruses in Vertebrate Cell Cultures.- 4. Infections by Flaviviruses in Vertebrate Cell Cultures.- 4.1. Acute Infection.- 4.2. Persistent Infection.- 5. Infection by Togaviruses in Invertebrate Cell Cultures.- 5.1. Acute Infection.- 5.2. Persistent Infection.- 6. Concluding Remarks.- 7. References.- Cumulative Contents.- Cumulative Author Index.- Cumulative Subject Index.



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