Molecular Analysis of DNA Rearrangements in the Immune System
The vertebrate immune system is distinctive among defense systems of multicellular organisms. In addition to nonspecific immunity, it generates a randomized array of millions of antigen receptors (immunoglobulins and T-cell receptors). A subset of these r
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Editors R.W. Compans. Atlanta/Gorgia M. Cooper. Birmingham/Alabama· H. Koprowski. Philadelphia/Pennsylvania . F. Melchers. Basel M. Oldstone. La Jolla/California· S. Olsnes. Oslo M. Potter. Bethesda/Maryland· H. Saedler. Cologne P. K. Vogt. La Jolla/Californa . H. Wagner. Munich
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Molecular Analysis of DNA Rearrangements in the Immune System Edited by R. Jessberger and M.R. Lieber
With 43 Figures and 13 Tables
Springer
DR. ROLF JESSBERGER
Institute for Immunology Grenzacherstr. 487 CH-4005 Basel Switzerland DR. MiCHAEL R. LIEBER
Division of Molecular Oncology Department of Pathology Washington University School of Medicine Campus Box 8118, 660 So. Euclid Ave. St. Louis, MO 63110 USA Cover illustration: V(D)J recombination is one of three covalent alterations of DNA that generate the genes encoding antigen receptors of the immune system. Class switch recombination and somatic hypermutation are two others. All three, and related topics, are discussed in this volume. The cover is a partial model for V(D)J recombination. The yellow circles represent the RAG-7,-2 endonuclease. This endonuclease cleaves at heptamer/nonamer signal sequences that have either a 72- or 23- base pair spacer between the heptamer and the nona mer (green and red triangles, respectively). The endonuclease generates a hairpinned coding end and a blunt signal end. Ku70/BO, a heterodimer, is the predominant DNA end binding protein in cells and is thought to bind to DNA termini. In one model, Ku is the DNA binding component of a complex that includes the DNA-dependent protein kinase, DNA-PKcs. DNA-PKcs appears to be the defective component in the doublestrand break repair complementation group XRCC7. XRCC7 also is the complementation group for murine SCID. Ku70 is defective in XRCC6, KuBO is defective in XRCC5. In V(D)J recombination, the signal ends are joined to form a signal joint. The V and J sub-exons are joined to form the coding joint, creating a novel exon in the immune-specific repertoire armamentarium. Cover design: Springer-Verlag Heidelberg, Design & Production ISSN 0070-217X ISBN 978-3-642-50142-5 ISBN 978-3-642-50140-1 (eBook) 00110.1007/978-3-642-50140-1 This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other way, and storage in data banks. Duplication of this publication or parts thereof is permitted only under the provisions of the German Copyright Law of September 9, 1965, in its current version, and permission for use must always be obtained from Springer-Verlag. Violations are liable for prosecution under the German Copyright Law.
© Springer-Verlag Berlin Heidelberg 1996 Library of Congress Catalog Card Number 15-12910 Softcover reprint of the hardcover 1st edition 1996 The this that and
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