ArticleJournal of virology2000
The LMP2A ITAM is essential for providing B cells with development and survival signals in vivo.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 123 citations in OpenAlex.
- A role for the protease MALT1 in EBV-mediated B-cell transformation by Latent Membrane Proteins 1 and 2.Leukemia · 2026Article
- Epstein-Barr Virus Latent Membrane Protein 2A (LMP2A) Enhances ATP Production in B Cell Tumors through mTOR and HIF-1α.International journal of molecular sciences · 2024Article
- Cancers associated with human gammaherpesviruses.The FEBS journal · 2022Review
- The impact of Epstein-Barr virus latent membrane protein 2A on the production of B cell activating factor of the tumor necrosis factor family (BAFF), APRIL and their receptors.Immunity, inflammation and disease · 2022Article
- Latent membrane proteins from EBV differentially target cellular pathways to accelerate MYC-induced lymphomagenesis.Blood advances · 2022Article
- Strategies of Epstein-Barr virus to evade innate antiviral immunity of its human host.Frontiers in microbiology · 2022Review
- Stress-Induced Epstein-Barr Virus Reactivation.Biomolecules · 2021Review
- Developmental partitioning of SYK and ZAP70 prevents autoimmunity and cancer.Molecular cell · 2021Article
- Molecular Interactions between Two LMP2A PY Motifs of EBV and WW Domains of E3 Ubiquitin Ligase AIP4.Life (Basel, Switzerland) · 2021Article
- Hallmarks of Cancers: Primary Antibody DeficiencyFrontiers in immunology · 2021Review
- Potential anti-proliferative effects of chemical constituents and hemisynthetic derivatives fromAfrican health sciences · 2020Article
- Epstein Barr Virus Associated Lymphomas and Epithelia Cancers in Humans.Journal of Cancer · 2020Review
- Oncogenic Epstein-Barr virus recruits Nm23-H1 to regulate chromatin modifiers.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Autoimmunity checkpoints as therapeutic targets in B cell malignancies.Nature reviews. Cancer · 2018Review
- EBV latent membrane protein 2A orchestrates p27Blood · 2017Article
- Interferon-γ-inducible protein 16 (IFI16) is required for the maintenance of Epstein-Barr virus latency.Virology journal · 2017Article
- Current Progress in EBV-Associated B-Cell Lymphomas.Advances in experimental medicine and biology · 2017Review
- Manipulation of the host cell membrane by human γ-herpesviruses EBV and KSHV for pathogenesis.Virologica Sinica · 2016Review
- Epstein-Barr Virus: Diseases Linked to Infection and Transformation.Frontiers in microbiology · 2016Review
- Epstein-Barr virus Latent Membrane Protein 2A (LMP2A)-mediated changes in Fas expression and Fas-dependent apoptosis: Role of Lyn/Syk activation.Cellular immunology · 2015Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In Epstein-Barr virus-transformed B cells, known as lymphoblastoid cell lines (LCLs), LMP2A binds the tyrosine kinases Syk and Lyn, blocking B-cell receptor (BCR) signaling and viral lytic replication. SH2 domains in Syk mediate binding to a phosphorylated immunoreceptor tyrosine-based activation motif (ITAM) in LMP2A. Mutation of the LMP2A ITAM in LCLs eliminates Syk binding and allows for full BCR signaling, thereby delineating the significance of the LMP2A-Syk interaction. In transgenic mice, LMP2A causes a developmental alteration characterized by a block in surface immunoglobulin rearrangement resulting in BCR-negative B cells. Normally B cells lacking cognate BCR are rapidly apoptosed; however, LMP2A transgenic B cells develop and survive without a BCR. When bred into the recombinase activating gene 1 null (RAG(-/-)) background, all LMP2A transgenic lines produce BCR-negative B cells that develop and survive in the periphery. These data indicate that LMP2A imparts developmental and survival signals to B cells in vivo. In this study, LMP2A ITAM mutant transgenic mice were generated to investigate whether the LMP2A ITAM is essential for the survival phenotype in vivo. LMP2A ITAM mutant B cells develop normally, although transgene expression is comparable to that in previously described nonmutated LMP2A transgenic B cells. Additionally, LMP2A ITAM mutant mice are unable to promote B-cell development or survival when bred into the RAG(-/-) background or when grown in methylcellulose containing interleukin-7. These data demonstrate that the LMP2A ITAM is required for LMP2A-mediated developmental and survival signals in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.