Epstein-Barr virus LMP2A drives B cell development and survival in the absence of normal B cell receptor signals.

[1]  D. Thorley-Lawson,et al.  EBV persistence in memory B cells in vivo. , 1998, Immunity.

[2]  K. Rajewsky,et al.  In Vivo Ablation of Surface Immunoglobulin on Mature B Cells by Inducible Gene Targeting Results in Rapid Cell Death , 1997, Cell.

[3]  R. Longnecker,et al.  The immunoreceptor tyrosine-based activation motif of Epstein-Barr virus LMP2A is essential for blocking BCR-mediated signal transduction. , 1997, Virology.

[4]  K. Rajewsky,et al.  Hodgkin and Reed-Sternberg cells in lymphocyte predominant Hodgkin disease represent clonal populations of germinal center-derived tumor B cells. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[5]  D. Thorley-Lawson,et al.  Identification of the site of Epstein-Barr virus persistence in vivo as a resting B cell , 1997 .

[6]  K. Rajewsky,et al.  Hodgkin and Reed-Sternberg cells in Hodgkin's disease represent the outgrowth of a dominant tumor clone derived from (crippled) germinal center B cells , 1996, The Journal of experimental medicine.

[7]  E. Kremmer,et al.  Identification of latent membrane protein 2A (LMP2A) domains essential for the LMP2A dominant-negative effect on B-lymphocyte surface immunoglobulin signal transduction , 1996, Journal of virology.

[8]  Victor L. J. Tybulewicz,et al.  Perinatal lethality and blocked B-cell development in mice lacking the tyrosine kinase Syk , 1995, Nature.

[9]  Tony Pawson,et al.  Syk tyrosine kinase required for mouse viability and B-cell development , 1995, Nature.

[10]  G. Winberg,et al.  A subpopulation of normal B cells latently infected with Epstein-Barr virus resembles Burkitt lymphoma cells in expressing EBNA-1 but not EBNA-2 or LMP1 , 1995, Journal of virology.

[11]  Y. Takahama,et al.  Regulation of early T cell development by the engagement of TCR-beta complex expressed on fetal thymocytes from TCR-beta-transgenic scid mice. , 1995, Journal of immunology.

[12]  D. Thorley-Lawson,et al.  A novel form of Epstein-Barr virus latency in normal B cells in vivo , 1995, Cell.

[13]  E. Kieff,et al.  Integral membrane protein 2 of Epstein-Barr virus regulates reactivation from latency through dominant negative effects on protein-tyrosine kinases. , 1995, Immunity.

[14]  L. Young,et al.  Epstein-Barr virus latency in blood mononuclear cells: analysis of viral gene transcription during primary infection and in the carrier state , 1994, Journal of virology.

[15]  D. Baltimore,et al.  Functional immunoglobulin transgenes guide ordered B-cell differentiation in Rag-1-deficient mice. , 1994, Genes & development.

[16]  E. Kieff,et al.  An integral membrane protein (LMP2) blocks reactivation of Epstein-Barr virus from latency following surface immunoglobulin crosslinking. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[17]  E. Kieff,et al.  Deletion of DNA encoding the first five transmembrane domains of Epstein-Barr virus latent membrane proteins 2A and 2B , 1993, Journal of virology.

[18]  E. Kieff,et al.  Epstein-Barr virus latent membrane protein 2A blocks calcium mobilization in B lymphocytes , 1993, Journal of virology.

[19]  E. Kieff,et al.  The last seven transmembrane and carboxy-terminal cytoplasmic domains of Epstein-Barr virus latent membrane protein 2 (LMP2) are dispensable for lymphocyte infection and growth transformation in vitro , 1993, Journal of virology.

[20]  R. Longnecker,et al.  Marker rescue of a transformation-negative Epstein-Barr virus recombinant from an infected Burkitt lymphoma cell line: a method useful for analysis of genes essential for transformation , 1993, Journal of virology.

[21]  E. Kieff,et al.  The only domain which distinguishes Epstein-Barr virus latent membrane protein 2A (LMP2A) from LMP2B is dispensable for lymphocyte infection and growth transformation in vitro; LMP2A is therefore nonessential , 1992, Journal of virology.

[22]  E. Kieff,et al.  An Epstein-Barr virus transformation-associated membrane protein interacts with src family tyrosine kinases , 1992, Journal of virology.

[23]  D. Rowe,et al.  Epstein-Barr virus latent gene expression in uncultured peripheral blood lymphocytes , 1992, Journal of virology.

[24]  V. Stewart,et al.  RAG-2-deficient mice lack mature lymphocytes owing to inability to initiate V(D)J rearrangement , 1992, Cell.

[25]  Susumu Tonegawa,et al.  RAG-1-deficient mice have no mature B and T lymphocytes , 1992, Cell.

[26]  A. Rolink,et al.  Molecular and cellular origins of B lymphocyte diversity , 1991, Cell.

[27]  E. Kieff,et al.  An Epstein-Barr virus protein associated with cell growth transformation interacts with a tyrosine kinase , 1991, Journal of virology.

[28]  A. Rickinson,et al.  Spontaneous outgrowth of epstein‐barr virus‐positive B‐cell lines from circulating human B cells of different buoyant densities , 1991, International journal of cancer.

[29]  H. Whittle,et al.  Circulating Epstein-Barr virus-carrying B cells in acute malaria , 1991, The Lancet.

[30]  Klaus Rajewsky,et al.  A B cell-deficient mouse by targeted disruption of the membrane exon of the immunoglobulin μ chain gene , 1991, Nature.

[31]  D. Baltimore,et al.  Virus-transformed pre-B cells show ordered activation but not inactivation of immunoglobulin gene rearrangement and transcription , 1991, The Journal of experimental medicine.

[32]  J. Miyazaki,et al.  Differentiation of growth signal requirement of B lymphocyte precursor is directed by expression of immunoglobulin. , 1991, The EMBO journal.

[33]  E. Kieff,et al.  A second Epstein-Barr virus membrane protein (LMP2) is expressed in latent infection and colocalizes with LMP1 , 1990, Journal of virology.

[34]  D. Baltimore,et al.  Activation of immunoglobulin kappa gene rearrangement correlates with induction of germline kappa gene transcription , 1989, Cell.

[35]  M. Rowe,et al.  Epstein‐barr virus‐infected b cells persist in the circulation of acyclovir‐treated virus carriers , 1989, International journal of cancer.

[36]  I. Ernberg,et al.  Eradication of Epstein-Barr virus by allogeneic bone marrow transplantation: implications for sites of viral latency. , 1988, Proceedings of the National Academy of Sciences of the United States of America.

[37]  H. Strander,et al.  Characterization of ebv‐carrying b‐cell populations in healthy seropositive individuals with regard to density, release of transforming virus and spontaneous outgrowth , 1987, International journal of cancer.

[38]  R. Grosschedl,et al.  Cell-type specificity of iminunoglobulin gene expression is regulated by at least three DNA sequence elements , 1985, Cell.

[39]  J. Sikela,et al.  Nucleotide sequence and organization of the mouse adenine phosphoribosyltransferase gene: presence of a coding region common to animal and bacterial phosphoribosyltransferases that has a variable intron/exon arrangement. , 1985, Proceedings of the National Academy of Sciences of the United States of America.

[40]  M. Epstein,et al.  A re‐examination of the epstein‐barr virus carrier state in healthy seropositive individuals , 1985, International journal of cancer.

[41]  T. Honjo,et al.  Epstein–Barr virus transforms precursor B cells even before immunoglobulin gene rearrangements , 1984, Nature.

[42]  R. Longnecker,et al.  Regulation of Epstein-Barr virus latency by latent membrane protein 2. , 1996, Trends in microbiology.

[43]  E. Kieff.  Epstein-Barr virus and its replication , 1996 .