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Mechanisms of Lymphocyte Activation and Immune Regulation XI [electronic resource] : B Cell Biology / edited by Sudhir Gupta, Frederick Alt, Max Cooper, Fritz Melchers, Klaus Rajewsky.

Por: Colaborador(es): Tipo de material: TextoTextoSeries Advances in Experimental Medicine and Biology ; 596 | Advances in Experimental Medicine and Biology ; 596Editor: Boston, MA : Springer US, 2007Descripción: X, 198 p. 44 illus. online resourceTipo de contenido:
  • text
Tipo de medio:
  • computer
Tipo de soporte:
  • online resource
ISBN:
  • 9780387465302
Trabajos contenidos:
  • SpringerLink (Online service)
Tema(s): Formatos físicos adicionales: Sin títuloClasificación CDD:
  • 616.079 23
Clasificación LoC:
  • QR180-189.5
Recursos en línea:
Contenidos:
Springer eBooksResumen: In recent years, major developments have been made in understanding various genetic and epigenetic regulatory processes that are critical for the generation of B cell repertoires. These include the role of chromatin regulation and nuclear organization in understating the IgH gene regulation. A role and mechanism of DNA repair proteins in somatic hypermutation has been elucidated. Genetic mutation studies have been instrumental in providing insight into some of the mechanisms involved in targeting CSR to various switch DNA regions located upstream of C region genes, especially a role of AID motifs, transcription, and R-loops. Recent studies support a dominant role of receptor editing in central B cell tolerance and signaling pathways that regulate receptor editing in self-reactive and non-self-reactive immature B cells. These were some of the topics of discussion at the 11th International Conference on B cell Biology. These proceedings highlight recent developments in lymphocyte development, Ig gene rearrangements and somatic hypermutation, chromatin structure modification, B lymphocyte signaling and fate, receptor editing, and autoimmunity.
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Regulation and Function of the E2A Proteins in B Cell Development -- Multiple Roles for Blimp-1 in B and T Lymphocytes -- Memory B Cell Evolution: B Cell Biology -- BCR-linked Factors in Developmental Fate Decisions -- Gene Regulatory Networks that Orchestrate the Development of B Lymphocyte Precursors -- Rules for the Rearrangement Events at the L Chain Gene Loci of the Mouse -- Regulation of AID Function In Vivo -- Targeting of AID to Immunoglobulin Genes -- Targeting AID to the Ig Genes -- DNA Replication to Aid Somatic Hypermutation -- Regulation of Activation Induced Deaminase via Phosphorylation -- Modulation of MHC Class II Signal Transduction by CD19 -- Role of NFUP?B Signaling in Normal and Malignant B Cell Development -- Fc Receptorlike Proteins (FCRL): Immunomodulators of B Cell Function -- Tolerance Mechanisms in the Late Phase of the Antibody Response -- Role of RS/?DE in B Cell Receptor Editing -- The Regulation of Receptor Editing -- B Cell Hyporesponsiveness and Autoimmunity: A New Paradigm.

In recent years, major developments have been made in understanding various genetic and epigenetic regulatory processes that are critical for the generation of B cell repertoires. These include the role of chromatin regulation and nuclear organization in understating the IgH gene regulation. A role and mechanism of DNA repair proteins in somatic hypermutation has been elucidated. Genetic mutation studies have been instrumental in providing insight into some of the mechanisms involved in targeting CSR to various switch DNA regions located upstream of C region genes, especially a role of AID motifs, transcription, and R-loops. Recent studies support a dominant role of receptor editing in central B cell tolerance and signaling pathways that regulate receptor editing in self-reactive and non-self-reactive immature B cells. These were some of the topics of discussion at the 11th International Conference on B cell Biology. These proceedings highlight recent developments in lymphocyte development, Ig gene rearrangements and somatic hypermutation, chromatin structure modification, B lymphocyte signaling and fate, receptor editing, and autoimmunity.

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