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  • 1
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    Response to RAG-mediated VDJ cleavage by NBS1 and gamma-H2AX (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-09
    Description: Genetic disorders affecting cellular responses to DNA damage are characterized by high rates of translocations involving antigen receptor loci and increased susceptibility to lymphoid malignancies. We report that the Nijmegen breakage syndrome protein (NBS1) and histone gamma-H2AX, which associate with irradiation-induced DNA double-strand breaks (DSBs), are also found at sites of VDJ (variable, diversity, joining) recombination-induced DSBs. In developing thymocytes, NBS1 and gamma-H2AX form nuclear foci that colocalize with the T cell receptor alpha locus in response to recombination activating gene (RAG) protein-mediated VDJ cleavage. Our results suggest that surveillance of T cell receptor recombination intermediates by NBS1 and gamma-H2AX may be important for preventing oncogenic translocations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721589/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721589/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, H T -- Bhandoola, A -- Difilippantonio, M J -- Zhu, J -- Brown, M J -- Tai, X -- Rogakou, E P -- Brotz, T M -- Bonner, W M -- Ried, T -- Nussenzweig, A -- Z99 CA999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 8;290(5498):1962-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11110662" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Nucleus/metabolism ; DNA Damage ; DNA-Binding Proteins/metabolism ; Fluorescent Antibody Technique ; *Gene Rearrangement, alpha-Chain T-Cell Antigen Receptor ; *Genes, T-Cell Receptor alpha ; Histones/*metabolism ; Homeodomain Proteins/metabolism ; Mice ; Mice, Transgenic ; Microscopy, Confocal ; Molecular Sequence Data ; Nuclear Proteins/*metabolism ; Phosphorylation ; *Recombination, Genetic ; T-Lymphocytes/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Contribution of receptor editing to the antibody repertoire (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-02-27
    Description: Receptor editing, clonal deletion, and anergy are the mechanisms by which B cells maintain tolerance to self antigens. To determine the extent to which receptor editing shapes the normal antibody repertoire, we generated an immunoglobulin kappa polymorphism that facilitates the detection of editing of immunoglobulin light chains in vivo. We found that B cells are targeted for editing during a 2-hour delay in development at the pre-BII cell stage, and that about 25% of all antibody molecules are produced by gene replacement. These results suggest that receptor editing represents a major force in shaping the antibody repertoire.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Casellas, R -- Shih, T A -- Kleinewietfeld, M -- Rakonjac, J -- Nemazee, D -- Rajewsky, K -- Nussenzweig, M C -- 33890/PHS HHS/ -- R01 AI033608/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2001 Feb 23;291(5508):1541-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, Howard Hughes Medical Institute, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11222858" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Affinity ; B-Lymphocytes/*immunology/metabolism ; Binding Sites, Antibody ; DNA-Binding Proteins/genetics/metabolism ; *Gene Rearrangement, B-Lymphocyte, Light Chain ; Genes, Immunoglobulin ; Hematopoietic Stem Cells/cytology/immunology ; Humans ; Immunoglobulin Constant Regions/genetics ; Immunoglobulin Heavy Chains/genetics ; Immunoglobulin kappa-Chains/genetics/immunology ; Mice ; Mice, Transgenic ; Models, Immunological ; Nuclear Proteins ; Receptors, Antigen, B-Cell/*genetics/*immunology ; Recombination, Genetic ; *Self Tolerance
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Coordinate regulation of RAG1 and RAG2 by cell type-specific DNA elements 5' of RAG2 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-14
    Description: RAG1 and RAG2 are essential for V(D)J recombination and lymphocyte development. These genes are thought to encode a transposase derived from a mobile genetic element that was inserted into the vertebrate genome 450 million years ago. The regulation of RAG1 and RAG2 was investigated in vivo with bacterial artificial chromosome (BAC) transgenes containing a fluorescent indicator. Coordinate expression of RAG1 and RAG2 in B and T cells was found to be regulated by distinct genetic elements found on the 5' side of the RAG2 gene. This observation suggests a mechanism by which asymmetrically disposed cis DNA elements could influence the expression of the primordial transposon and thereby capture RAGs for vertebrate evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, W -- Misulovin, Z -- Suh, H -- Hardy, R R -- Jankovic, M -- Yannoutsos, N -- Nussenzweig, M C -- GM07739/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Aug 13;285(5430):1080-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10446057" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*metabolism ; Bacterial Proteins/genetics ; DNA-Binding Proteins/*genetics ; *Gene Expression Regulation ; Genes, Immunoglobulin ; *Genes, RAG-1 ; Green Fluorescent Proteins ; Luminescent Proteins/genetics ; Mice ; Mice, Transgenic ; Recombinant Fusion Proteins ; Recombination, Genetic ; *Regulatory Sequences, Nucleic Acid ; Sequence Deletion ; T-Lymphocytes/*metabolism ; Transcription, Genetic ; Transgenes ; Transposases/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    The role of Ig beta in precursor B cell transition and allelic exclusion (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-04-21
    Description: Lymphocytes express multicomponent receptor complexes that mediate diverse antigen-dependent and antigen-independent responses. Despite the central role of antigen-independent events in B cell development, little is known about the mechanisms by which they are initiated. The association between the membrane immunoglobulin (Ig) M heavy chair (micron) and the Ig alpha-Ig beta heterodimer is now shown to be essential in inducing both the transition from progenitor to precursor B cells and subsequent allelic exclusion in transgenic mice. The cytoplasmic domain of Ig beta is sufficient to induce these early antigen-independent events by a mechanism that requires conserved tyrosine residues in this protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papavasiliou, F -- Misulovin, Z -- Suh, H -- Nussenzweig, M C -- AI33890/AI/NIAID NIH HHS/ -- AI37526/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1995 Apr 21;268(5209):408-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7716544" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; *Antigens, CD ; Antigens, CD79 ; B-Lymphocytes/cytology/*immunology ; Genes, Immunoglobulin ; Humans ; Immunoglobulin mu-Chains/metabolism ; Immunoglobulins/*metabolism ; Lymphocyte Activation ; Membrane Glycoproteins/*metabolism ; Mice ; Mice, Transgenic ; Receptors, Antigen, B-Cell/*metabolism ; Recombination, Genetic ; Signal Transduction ; Tyrosine/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Differential antigen processing by dendritic cell subsets in vivo (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-01-06
    Description: Dendritic cells (DCs) process and present self and foreign antigens to induce tolerance or immunity. In vitro models suggest that induction of immunity is controlled by regulating the presentation of antigen, but little is known about how DCs control antigen presentation in vivo. To examine antigen processing and presentation in vivo, we specifically targeted antigens to two major subsets of DCs by using chimeric monoclonal antibodies. Unlike CD8+ DCs that express the cell surface protein CD205, CD8- DCs, which are positive for the 33D1 antigen, are specialized for presentation on major histocompatibility complex (MHC) class II. This difference in antigen processing is intrinsic to the DC subsets and is associated with increased expression of proteins involved in MHC processing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dudziak, Diana -- Kamphorst, Alice O -- Heidkamp, Gordon F -- Buchholz, Veit R -- Trumpfheller, Christine -- Yamazaki, Sayuri -- Cheong, Cheolho -- Liu, Kang -- Lee, Han-Woong -- Park, Chae Gyu -- Steinman, Ralph M -- Nussenzweig, Michel C -- New York, N.Y. -- Science. 2007 Jan 5;315(5808):107-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, The Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17204652" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/immunology ; *Antigen Presentation ; Antigens, CD/analysis/immunology ; Antigens, CD8/analysis/immunology ; Base Sequence ; Dendritic Cells/*immunology ; Histocompatibility Antigens Class I/immunology ; Histocompatibility Antigens Class II/immunology ; Lectins, C-Type/analysis/immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Transgenic ; Molecular Sequence Data ; Oligonucleotide Array Sequence Analysis ; Receptors, Cell Surface/analysis/immunology ; T-Lymphocytes/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    HUMORAL IMMUNITY. T cell help controls the speed of the cell cycle in germinal center B cells (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-07-18
    Description: The germinal center (GC) is a microanatomical compartment wherein high-affinity antibody-producing B cells are selectively expanded. B cells proliferate and mutate their antibody genes in the dark zone (DZ) of the GC and are then selected by T cells in the light zone (LZ) on the basis of affinity. Here, we show that T cell help regulates the speed of cell cycle phase transitions and DNA replication of GC B cells. Genome sequencing and single-molecule analyses revealed that T cell help shortens S phase by regulating replication fork progression, while preserving the relative order of replication origin activation. Thus, high-affinity GC B cells are selected by a mechanism that involves prolonged dwell time in the DZ where selected cells undergo accelerated cell cycles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gitlin, Alexander D -- Mayer, Christian T -- Oliveira, Thiago Y -- Shulman, Ziv -- Jones, Mathew J K -- Koren, Amnon -- Nussenzweig, Michel C -- 1F30AI109903-01/AI/NIAID NIH HHS/ -- 1UM1 AI100663-01/AI/NIAID NIH HHS/ -- AI037526-19/AI/NIAID NIH HHS/ -- AI072529-06/AI/NIAID NIH HHS/ -- T32GM07739/GM/NIGMS NIH HHS/ -- UM1 AI100663/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Aug 7;349(6248):643-6. doi: 10.1126/science.aac4919. Epub 2015 Jul 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA. ; Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA. ; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Laboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA. Howard Hughes Medical Institute (HHMI), The Rockefeller University, New York, NY 10065, USA. nussen@rockefeller.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26184917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*cytology ; Cell Cycle/genetics/*immunology ; Cell Proliferation ; DNA Replication/genetics/*immunology ; Gene Expression Regulation ; Germinal Center/*cytology ; Immunity, Humoral/*genetics ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; S Phase/genetics/immunology ; T-Lymphocytes/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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