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Advances in genetics Volume 82 /
The field of genetics is rapidly evolving, and new medical breakthroughs are occurring as a result of advances in our knowledge of genetics. This series continually publishes important reviews of the broadest interest to geneticists and their colleagues in affiliated disciplines. * Includes methods...
| Clasificación: | Libro Electrónico |
|---|---|
| Otros Autores: | , , |
| Formato: | Electrónico eBook |
| Idioma: | Inglés |
| Publicado: |
Amsterdam, Netherlands :
Elsevier,
�2013.
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| Temas: | |
| Acceso en línea: | Texto completo |
Tabla de Contenidos:
- Front Cover; Advances in Genetics; Copyright; Contents; Contributors; Chapter One: The Repair and Signaling Responses to DNA Double-Strand Breaks; 1. Introduction; 2. Formation of DSBs; 3. Mechanisms of DSB Rejoining; 3.1. Homologous recombination; 3.2. Nonhomologous end-joining; 3.2.1. DNA-PK: The first complex formed during NHEJ; 3.2.2. DSB end processing during NHEJ; 3.2.3. DNA ligase IV, XRCC4, and XLF, the second NHEJ complex; 3.3. Additional end-joining processes; 4. DNA Damage Response Signaling; 4.1. The assembly process; 4.2. Factors regulating the recruitment of 53BP1
- 4.3. Assembly of the BRCA1 and the RAP80/Abraxas/BRCC36 complex4.4. Involvement of noncoding RNAs; 5. Functions of the DDR Assembly; 5.1. Signaling to the checkpoint machinery; 5.2. The repair of DSB located within heterochromatin; 5.3. Transcriptional arrest at transcriptionally active DSBs; 5.4. Impact of additional chromatin changes at DSBs; 5.4.1. Role for HP1 in the DDR; 5.4.2. The involvement of CHD4-NuRD in the DDR; 5.4.3. The involvement of Tip60 and the NuA4 complex in the DDR; 5.4.4. The involvement of SNF2H, ACF1, and RNF20-RNF40 in the DDR
- 6. Regulation of DSB Repair Pathway Choice6.1. Impact of cell cycle phase and resection; 6.2. Role of 53BP1; 6.3. Model for the interface between NHEJ and HR; 7. Contribution of Defects in DSB Rejoining Processes to Human Disease; 8. Concluding Remarks; References; Chapter Two: Biological Activity and Biotechnological Aspects of Locked Nucleic Acids; 1. Brief Introduction; 2. Chemistry and Structure; 2.1. LNA characteristics and structure; 2.2. LNA analogues and conjugates; 3. Biological Activity of LNA-Containing ONs; 3.1. Antisense LNA; 3.1.1. Affinity and potency
- 3.1.2. Cellular uptake and gymnosis3.1.2.1. Uptake mechanisms; 3.1.2.2. Comparing cellular uptake and antisense efficiency; 3.2. siLNA: Improving siRNA performance by LNA modification; 3.2.1. Tolerance for LNA modification; 3.2.2. Enhancing siRNA activity and specificity by LNA modification; 3.2.3. Enhancing siRNA nuclease resistance by LNA modification; 3.2.4. Reducing siRNA immunogenicity by LNA modification; 3.2.5. Applying siLNA in vivo; 3.3. LNA and splice-switching ONs; 3.3.1. Splice switching; 3.3.2. LNA in SSOs; 3.4. LNA in antigene reagents; 3.4.1. LNA in triplex-forming ONs
- 3.4.1.1. LNA-modified pyrimidine TFOs3.4.1.2. Intracellular effects of LNA-modified pyrimidine TFOs; 3.4.2. LNA in double-strand-invading ONs; 3.4.2.1. LNA-containing clamp ONs; 3.4.2.2. Invader-LNA; 3.4.2.3. Zorro-LNA; 3.4.2.4. ``Linear� � antigene LNA ONs; 4. LNA Pharmacology; 4.1. Pharmacokinetics; 4.1.1. Delivery and bioavailability; 4.1.2. Tissue distribution; 4.2. Pharmacodynamics; 4.2.1. Targeting ApoB-100; 4.2.2. Targeting PCSK9; 4.2.3. Targeting miR-122; 4.2.4. LNA pharmacology in malignant tissues; 5. LNA in Biotechnology; 5.1. LNA in primers and probes; 5.1.1. LNA primers