Advances in genetics. Volume 90 /

The field of genetics is rapidly evolving, and new medical breakthroughs are occurring as a result of advances in our knowledge of genetics. Advances in Genetics continually publishes important reviews of the broadest interest to geneticists and their colleagues in affiliated disciplines. <li>...

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Bibliographic Details
Corporate Author: ScienceDirect (Online service)
Format: eBook
Language:English
Published: San Diego : Elsevier Academic Press, 2015.
Series:Advances in genetics ; v. 90.
Subjects:
Online Access:Connect to the full text of this electronic book
Table of Contents:
  • Genetics and Pharmacology of Longevity: The Road to Therapeutics for Healthy Aging
  • 1. Introduction
  • 2. Molecular Genetics of Aging
  • 2.1. Molecular Mechanisms of Aging
  • 2.1.1. Dysfunctional Molecular Fidelity as a Driver of Aging
  • 2.1.1.1. DNA Damage, Telomere Attrition, and Stem Cell Maintenance
  • 2.1.1.2. Proteostasis: Protein Quality Control
  • 2.1.2. Cellular Responses to Molecular Damage and Stress
  • 2.2. DR and the Nutrient-Sensing Network
  • 2.2.1. The Physiology of Nutrient Sensing
  • 2.2.1.1. Insulin and IGF Signaling
  • 2.2.1.2. mTOR and the Integration of Nutrient Sensing
  • 2.2.1.3. Downstream of mTOR: S6K, 4E-BP, and atg1/ULK1
  • 2.2.1.4. mTOR and mTOR-Independent Mechanisms of Nutrient Sensing
  • 2.2.2. Genetics of IIS, mTOR, and AMPK for Aging: From Caenorhabditis elegans to Mammals
  • 2.2.2.1. IIS Longevity in Model Organisms
  • 2.2.2.2. mTORC1 Regulation of Longevity
  • 2.2.2.3. Energy Regulation and AMPK in Longevity
  • 2.2.2.4. Transcriptional Regulation of Longevity
  • 2.2.2.5. miRNAs in Longevity, Health, and Disease
  • 2.3. Human Aging: The Genome-Wide Approach
  • 3. Pharmacology of Aging
  • 3.1. Searching for a DR Mimetic
  • 3.2. Drugs in Aging: The Role of Model Organisms
  • 3.2.1. Rapamycin and Rapalogs
  • 3.2.2. Metformin and the Microbiota: Opening a can of Worms
  • 3.2.3. Drugs that Regulate Proteostasis through Autophagy
  • 3.2.4. Antioxidants in Aging
  • 3.2.5. Resveratrol and Sirtuins
  • 3.2.6. Disease-Modifying Drugs: Healthspan as a Target
  • 3.2.7. Targeting Molecular Fidelity for Healthy Aging with Drugs
  • 3.3. Pharmacogenetics and Pharmacogenomics: Candidate Approach versus Established Drugs
  • 4. Therapeutics of Aging
  • 4.1. Targets of Aging Research: Life Span versus Healthspan
  • 4.2. Combination of Interventions for Aging: The Road for a Polypill
  • 4.2.1. Epistasis between DR and the Nutrient-Sensing Network
  • 4.2.2. A Polypill for Aging
  • 4.3. The Aging Industry: Translating Pharmacology to Therapeutics
  • 5. Conclusions
  • MicroRNAs: Tools of Mechanistic Insights and Biological Therapeutics Discovery for the Rare Neurogenetic Syndrome Lesch-Nyh ...
  • 1. Introduction
  • 2. Lesch-Nyhan Disease: A Model Disease for Understanding Purine Metabolism Effect in the Brain
  • 3. MicroRNAs, Regulator of Neural Cell Function: A Pivotal Role in Neurodegenerative and Neurodevelopmental Diseases
  • 4. MicroRNAs and HPRT Deficiency
  • 4.1. miR-181a
  • 4.1.1. CREB
  • 4.2. miR-17
  • 4.3. miR-9
  • 4.3.1. Bcl11b
  • 4.3.2. FoxG1
  • 4.3.3. Neurotrophic Tyrosine Kinase Receptor 2
  • 4.4. miR-424
  • 4.4.1. Lmx1a and FoxA2
  • 5. Putative Role of Competitive RNAs in MicroRNA-Mediated Transcriptional Dysregulation in HPRT-Deficiency
  • 5.1. HPRT Transcript: A ceRNAs?
  • 6. Perspectives
  • 6.1. miRNA-Target Genes Interactions, Reliable Tools to Guide Biology Discovery for LND?
  • 6.2. Validating HPRT Deficiency-Mediated miRNAs Dysregulation in LND-Derived Brain Tissues
  • 6.3. miRNAs, Biomarkers for LND
  • 6.4. miRNAs, as Guide for Drug Repositioning Strategies for LND
  • Small RNAs in Bacteria and Archaea: Who They Are, What They Do, and How They Do It
  • 1. Introduction
  • 1.1. What We Will Not Cover
  • 1.2. What This Review is About
  • 2. sRNA Discovery-Who They Are
  • 2.1. In Enterobacteria
  • 2.2. And Elsewhere
  • 2.3. Not Only Intergenic ...
  • 3. Finding Targets and Functions
  • 3.1. Protein Sequestrators
  • 3.2. Finding Targets for Trans-Encoded sRNAs
  • 3.2.1. Biocomputational Strategies
  • 3.2.2. Experimental Strategies
  • 3.2.3. Addressing Mechanisms by In vitro Analyses
  • 4. What Are They Doing?
  • 4.1. Iron Homeostasis
  • 4.2. Membrane and Surface Remodeling
  • 4.3. Motility and Biofilm
  • 4.4. Regulation of Transporters
  • 4.5. Sugar Metabolism
  • 4.6. Regulating Transcription Factors for Various Responses
  • 4.7. sRNA Controlling Virulence Gene Expression
  • 4.8. sRNAs in Toxin-Antitoxin Systems
  • 4.9. And Much More ...
  • 5. And How?
  • 5.1. Modes of Action of sRNAs
  • 5.1.1. Inhibition by Direct Competition for the Ribosome Binding Site
  • 5.1.2. Translational Control via Ribosome Standby/Translational Enhancers
  • 5.1.3. Indirect Translational Regulation via Leader ORFs
  • 5.1.4. Activation of Translation
  • 5.1.5. RNA-Driven Transcriptional Attenuation
  • 5.1.6. Target RNA Degradation as a Secondary Effect
  • 5.1.7. Target RNA Degradation-Only Effects
  • 5.1.8. Stabilization of Target RNA
  • 5.1.9. Operon-Wide Effects via Induced Polarity
  • 5.1.10. RNA-Based Traps and Sponges
  • 5.1.11. Effects Through Recruitment of Proteins to mRNA
  • 5.1.12. Protein Sequestration
  • 5.2. Hfq-A Key Player in sRNA Control
  • 5.2.1. Hfq Binds Numerous RNAs
  • 5.2.2. Hfq Structure and Binding Surfaces
  • 5.2.3. RNA Binding and Promotion of sRNA-mRNA Pairing
  • 5.2.4. RNA Cycling on Hfq
  • 5.2.5. Hfq Variants and Other Proteins
  • 5.3. Pervasive Antisense Transcription-Noise or Function?
  • 5.3.1. Indications for Functions?
  • 5.3.2. Mechanisms toward Functions?
  • 6. Multitargeting and Interconnected Regulatory Networks
  • 7. sRNAs in Regulatory Motifs
  • 8. Specific Properties of sRNA Regulation
  • 9. Plasmid asRNAs Revisited-What They Taught Us and How They Compare to sRNAs
  • 9.1. Matching Biological Requirements with Properties of RNAs
  • 9.2. Favorable Structures and Topological Constraints
  • 9.3. Full Complementarity Does Not Mean Full Duplexes
  • 9.4. Hierarchically Ordered Binding Pathways
  • 9.5. Kinetics is Very Different from Repressor-type Control
  • 10. More of the Same, or Different?
  • 11. Why Are sRNAs Used Everywhere?
  • 12. Concluding Remarks.