Epstein-Barr Virus LMP2A Drives B Cell Development and Survival in the Absence of Normal B Cell Receptor Signals
Epstein-Barr virus (EBV) establishes a persistent latent infection in peripheral B lymphocytes in humans and is associated with a variety of malignancies and proliferative disorders. Latent membrane protein 2A (LMP2A) is one of only two viral proteins expressed in latently infected B lymphocytes in...
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Veröffentlicht in: | Immunity (Cambridge, Mass.) Mass.), 1998-09, Vol.9 (3), p.405-411 |
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description | Epstein-Barr virus (EBV) establishes a persistent latent infection in peripheral B lymphocytes in humans and is associated with a variety of malignancies and proliferative disorders. Latent membrane protein 2A (LMP2A) is one of only two viral proteins expressed in latently infected B lymphocytes in vivo. LMP2A blocks B cell receptor (BCR) signal transduction in vitro by binding the Syk and Lyn protein tyrosine kinases. To analyze the significance of LMP2A expression in vivo, transgenic mice with B cell lineage expression of LMP2A were generated. LMP2A expression results in the bypass of normal B lymphocyte developmental checkpoints allowing immunoglobulin-negative cells to colonize peripheral lymphoid organs, indicating that LMP2A possesses a constitutive signaling activity in nontransformed cells. |
doi_str_mv | 10.1016/S1074-7613(00)80623-8 |
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Latent membrane protein 2A (LMP2A) is one of only two viral proteins expressed in latently infected B lymphocytes in vivo. LMP2A blocks B cell receptor (BCR) signal transduction in vitro by binding the Syk and Lyn protein tyrosine kinases. To analyze the significance of LMP2A expression in vivo, transgenic mice with B cell lineage expression of LMP2A were generated. 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Latent membrane protein 2A (LMP2A) is one of only two viral proteins expressed in latently infected B lymphocytes in vivo. LMP2A blocks B cell receptor (BCR) signal transduction in vitro by binding the Syk and Lyn protein tyrosine kinases. To analyze the significance of LMP2A expression in vivo, transgenic mice with B cell lineage expression of LMP2A were generated. 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Wilson, Joanna B ; Anderson, Steven J ; Longnecker, Richard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c490t-fe5271e1b239f56850e8bdafb890b83918808c41ea3f74108f23f1d0460cf0953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Animals, Genetically Modified</topic><topic>B-Lymphocytes - cytology</topic><topic>B-Lymphocytes - virology</topic><topic>Bone Marrow Cells - cytology</topic><topic>Bone Marrow Cells - drug effects</topic><topic>Bone Marrow Cells - immunology</topic><topic>Cell Differentiation</topic><topic>Cell Survival</topic><topic>Cells, Cultured</topic><topic>Gene Rearrangement, B-Lymphocyte, Heavy Chain - drug effects</topic><topic>Gene Rearrangement, B-Lymphocyte, Heavy Chain - physiology</topic><topic>Genes, RAG-1 - physiology</topic><topic>Herpesvirus 4, Human - chemistry</topic><topic>Herpesvirus 4, Human - immunology</topic><topic>Interleukin-7 - pharmacology</topic><topic>Lymphocyte Activation - drug effects</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Receptors, Antigen, B-Cell - physiology</topic><topic>Signal Transduction</topic><topic>Transgenes - physiology</topic><topic>Viral Matrix Proteins - genetics</topic><topic>Viral Matrix Proteins - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Caldwell, Robert G</creatorcontrib><creatorcontrib>Wilson, Joanna B</creatorcontrib><creatorcontrib>Anderson, Steven J</creatorcontrib><creatorcontrib>Longnecker, Richard</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Immunity (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Caldwell, Robert G</au><au>Wilson, Joanna B</au><au>Anderson, Steven J</au><au>Longnecker, Richard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epstein-Barr Virus LMP2A Drives B Cell Development and Survival in the Absence of Normal B Cell Receptor Signals</atitle><jtitle>Immunity (Cambridge, Mass.)</jtitle><addtitle>Immunity</addtitle><date>1998-09-01</date><risdate>1998</risdate><volume>9</volume><issue>3</issue><spage>405</spage><epage>411</epage><pages>405-411</pages><issn>1074-7613</issn><eissn>1097-4180</eissn><abstract>Epstein-Barr virus (EBV) establishes a persistent latent infection in peripheral B lymphocytes in humans and is associated with a variety of malignancies and proliferative disorders. 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subjects | Animals Animals, Genetically Modified B-Lymphocytes - cytology B-Lymphocytes - virology Bone Marrow Cells - cytology Bone Marrow Cells - drug effects Bone Marrow Cells - immunology Cell Differentiation Cell Survival Cells, Cultured Gene Rearrangement, B-Lymphocyte, Heavy Chain - drug effects Gene Rearrangement, B-Lymphocyte, Heavy Chain - physiology Genes, RAG-1 - physiology Herpesvirus 4, Human - chemistry Herpesvirus 4, Human - immunology Interleukin-7 - pharmacology Lymphocyte Activation - drug effects Mice Mice, Inbred C57BL Mice, Transgenic Receptors, Antigen, B-Cell - physiology Signal Transduction Transgenes - physiology Viral Matrix Proteins - genetics Viral Matrix Proteins - physiology |
title | Epstein-Barr Virus LMP2A Drives B Cell Development and Survival in the Absence of Normal B Cell Receptor Signals |
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