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cover Advances in cancer research...
Advances in cancer research.
Academic Press 2012

Advances in Cancer Research provides invaluable information on the exciting and fast-moving field of cancer research. Here, once again, outstanding and original reviews are presented on a variety of topics. 113th volume of Advances in Cancer ResearchExpert authorsChapters on topics including microRNA regulatory network, multifaceted oncoprotein tax, and underlying chromosomal translocations

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Título:
Advances in cancer research. Volume 113 [ electronic resource] / edited by Kenneth D. Tew, Paul B. Fisher
Edición:
1st ed
Editorial:
San Diego, Calif. : Academic Press, 2012
Descripción física:
1 online resource (309 p.)
Mención de serie:
Advances in cancer research, 0065-230X ; v. 113
Nota general:
Description based upon print version of record
Bibliografía:
Includes bibliographical references and index
Contenido:
Front Cover; Advances in CANCER RESEARCH; Copyright; Contents; Contributors; Chapter 1: NaN: The AID Dilemma; I.Introduction; II. Two Distinct AID Functions; A. Phenotypes of AID Deficiency; B. Phenotypes of AID N-Terminal Mutations; C. Phenotypes of AID C-Terminal Mutations; III. DNA Cleavage Mechanism by AID; A. The DNA Deamination Hypothesis; 1. AID Deamination Activity; 2.UNG Involvement in CSR; 3.The AP Endonuclease (APE) Requirement; B. The RNA-Editing Model; 1. AID Induces DNA Cleavage by Reducing Top1; 2. CSR Depends on the Association of AID's C-Terminus with mRNA
C. AID Target Specificity for DNA Cleavage1.Non-Ig AID Targets; 2. Markers for AID Targets; IV. AID Involvement in Genome Instability and Tumorigenesis; A. Evolutionary Consideration of AID-Induced Genome Instability; 1.CSR and Meiotic Recombination Homology; 2.Top1 Involvement in Transcription-Related Genome Instability; B.Evidence for AID's Involvement in Tumorigenesis; 1. AID in Murine Tumors; 2. AID in GC-Derived B-Cell Lymphomas; 3. AID in non-GC-Derived B-Cell Lymphomas; 4. AID's Potential Importance in Human B-Cell Malignancies; C.Normal and Pathogen-Induced AID Expression
1.Pathogen-Induced AID Expression2.Regulation of AID Expression; V.Coda; Acknowledgments; References; Chapter 2: NaN: The MicroRNA Regulatory Network in Normal- and HTLV-1-Transformed T Cells; I.Introduction; A.miRNA Biogenesis; B.Consequences of miRNA-mRNA Interactions; II.HTLV-1 and ATLL; A.HTLV-1 Genome Organization and Expression; B.HTLV-1 Transmission and Persistence; C.ATLL and Other HTLV-1-Associated Diseases; III.miRNAs in Normal CD4+ T Cells; A.miRNA Profiles in T Cell Development; B.miRNAs in Activated T Cells; C.miRNAs in Tregs
IV.Cellular miRNA Expression in HTLV-1-Infected Cell LinesV.miRNA Profiling in ATLL Samples; VI.Repression of miR-31 Expression in ATLL; A.Identification of NF-kappaB-Inducing Kinase (NIK) as a Target of miR-31 in ATLL; B.Genetic Deletion and Polycomb-Directed Epigenetic Silencing Cause Loss of miR-31 Expression; C.The Polycomb Group Regulates NF-kappaB Activity by Controlling miR-31 Expression; VII.Perspectives; Acknowledgments; References; Chapter 3: NaN: The Multifaceted Oncoprotein Tax; I.The Oncogenic Retrovirus HTLV-I; II.The Viral Oncoprotein Tax: Structural and Functional Domains
III.Tax: A Potent Transactivator and a Deregulator of the Cellular MachineryIV.The NF-kappaB Pathway: Generalities; V.Tax: A Powerful Activator of the NF-kappaB Pathway; VI.Tax Posttranslational Modifications and NF-kappaB Activation; A.Tax Phosphorylation; B.Tax Acetylation; C.Tax Ubiquitination; D.Tax SUMOylation; VII.Tax Posttranslational Modifications and Intracellular Localization; VIII.Conclusion; Acknowledgments; References; Chapter 4: NaN: Lynch or Not Lynch? Is that Always a Question?; I.Introduction; II.What is HNPCC?; III.What is MSI?; IV.What is an MMR Defect?
V.What is Lynch Syndrome?
Lengua:
English
ISBN:
1-280-58269-3
9786613612472
0-12-397841-6
Materia:
Autores:
Enlace a serie principal:
Advances in cancer research (CKB)954926956844 (DLC)2011236561 (OCoLC)60625515 2162-5557
Enlace a formato físico adicional:
0-12-394280-2

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