| pubmed-article:10627520 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10627520 | lifeskim:mentions | umls-concept:C0014644 | lld:lifeskim |
| pubmed-article:10627520 | lifeskim:mentions | umls-concept:C0025936 | lld:lifeskim |
| pubmed-article:10627520 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
| pubmed-article:10627520 | lifeskim:mentions | umls-concept:C0456387 | lld:lifeskim |
| pubmed-article:10627520 | lifeskim:mentions | umls-concept:C1710548 | lld:lifeskim |
| pubmed-article:10627520 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:10627520 | pubmed:dateCreated | 2000-2-7 | lld:pubmed |
| pubmed-article:10627520 | pubmed:abstractText | Latent membrane protein 2A (LMP2A) is one of only two viral proteins expressed during latent Epstein-Barr virus (EBV) infections in human peripheral B cells. LMP2A blocks B-cell receptor (BCR) signal transduction in vitro by modulation of the Syk and Lyn protein tyrosine kinases. Five genetically unique LMP2A transgenic mouse lines (EmuLMP2A) with B-cell lineage expression of LMP2A were generated in this study to analyze the importance of LMP2A expression in vivo. These animals can be grouped into EmuLMP2A(BCR+) (TgB, Tg6, and TgC) and EmuLMP2A(BCR-) (Tg7 and TgE) lines based on B-cell phenotype. LMP2A expression in bone marrow cells of EmuLMP2A(BCR-) lines was associated with a bypass of normal B-lymphocyte developmental checkpoints inasmuch as immunoglobulin light-chain gene rearrangement occurred in the absence of complete immunoglobulin heavy-chain gene rearrangement. The resulting BCR-negative B cells were able to exit the bone marrow and colonize peripheral lymphoid organs. LMP2A expression in EmuLMP2A(BCR+) lines was not associated with altered B-cell development in a genetically wild-type background. When crossed into a recombinase activating null (RAG(-/-)) genetic background, LMP2A expression in either RAG(-/-) EmuLMP2A(BCR+) or RAG(-/-) EmuLMP2A(BCR-) animals was able to provide a survival signal to BCR-negative splenic B cells. Additionally, bone marrow cells from all EmuLMP2A animals were able to proliferate in response to interleukin-7-dependent developmental signals in vitro. These studies illustrate that LMP2A can provide a survival signal to BCR-negative B cells in two different groups of EmuLMP2A transgenic mice. | lld:pubmed |
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| pubmed-article:10627520 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10627520 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10627520 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10627520 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10627520 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:10627520 | pubmed:issn | 0022-538X | lld:pubmed |
| pubmed-article:10627520 | pubmed:author | pubmed-author:BrownR CRC | lld:pubmed |
| pubmed-article:10627520 | pubmed:author | pubmed-author:LongneckerRR | lld:pubmed |
| pubmed-article:10627520 | pubmed:author | pubmed-author:CaldwellR GRG | lld:pubmed |
| pubmed-article:10627520 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10627520 | pubmed:volume | 74 | lld:pubmed |
| pubmed-article:10627520 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10627520 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10627520 | pubmed:pagination | 1101-13 | lld:pubmed |
| pubmed-article:10627520 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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