ArticleProceedings of the National Academy of Sciences of the United States of America2009
Genetic evidence for the role of Erk activation in a lymphoproliferative disease of mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
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- The geroprotectors trametinib and rapamycin combine additively to extend mouse healthspan and lifespan.Nature aging · 2025Article
- Slow phosphorylation of a tyrosine residue in LAT optimizes T cell ligand discrimination.Nature immunology · 2019Article
- Lck promotes Zap70-dependent LAT phosphorylation by bridging Zap70 to LAT.Nature immunology · 2018Article
- Visualization of RAS/MAPK Signaling In Situ by the Proximity Ligation Assay (PLA).Methods in molecular biology (Clifton, N.J.) · 2017Article
- α-Melanocyte-stimulating hormone ameliorates ocular surface dysfunctions and lesions in a scopolamine-induced dry eye model via PKA-CREB and MEK-Erk pathways.Scientific reports · 2015Article
- Differential roles of hippocampal glutamatergic receptors in neuropathic anxiety-like behavior after partial sciatic nerve ligation in rats.BMC neuroscience · 2015Article
- miR-155 Controls Lymphoproliferation in LAT Mutant Mice by Restraining T-Cell Apoptosis via SHIP-1/mTOR and PAK1/FOXO3/BIM Pathways.PloS one · 2015Article
- The MAP kinase p38 is part of Drosophila melanogaster's circadian clock.PLoS genetics · 2014Article
- The characteristics of Bax inhibitor-1 and its related diseases.Current molecular medicine · 2014Review
- Ras and extracellular signal-regulated kinase signaling in thymocytes and T cells.Trends in immunology · 2013Review
- miRNA signature of mouse helper T cell hyper-proliferation.PloS one · 2013Article
- A phospholipase C-γ1-independent, RasGRP1-ERK-dependent pathway drives lymphoproliferative disease in linker for activation of T cells-Y136F mutant mice.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- LAT-independent Erk activation via Bam32-PLC-γ1-Pak1 complexes: GTPase-independent Pak1 activation.Molecular cell · 2012Article
- The importance of the Erk pathway in the development of linker for activation of T cells-mediated autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Multiple signaling pathways are involved in the interleukine-4 regulated expression of DC-SIGN in THP-1 cell line.Journal of biomedicine & biotechnology · 2012Article
- The LAT story: a tale of cooperativity, coordination, and choreography.Cold Spring Harbor perspectives in biology · 2010Review
- Impaired CD4+ T-cell proliferation and effector function correlates with repressive histone methylation events in a mouse model of severe sepsis.European journal of immunology · 2010Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Germline mutation of the linker for activation of T cells (LAT) gene at the phospholipase C-gamma1 (PLC-gamma1)-binding site leads to a fatal lymphoproliferative disease in mice. The hyperactivated T cells that develop in these mice have defective T-cell antigen receptor (TCR)-induced calcium flux but enhanced mitogen-activated protein kinase (MAPK) activation. We used genetic analysis to investigate genes whose products might suppress MAPK activation and lymphoproliferative disease in LAT mutant mice. B-lymphocyte adaptor molecule of 32 kDa (Bam32) is a known mediator of MAPK activation in B cells. We recently reported that in CD4(+) T cells, Bam32 deficiency decreased MAPK activation and specifically extracellular-signal-regulated kinase (Erk) signaling, following TCR stimulation. By crossing the Bam32 null mutation onto the LAT knock-in background, we found that the Bam32 null mutation delayed the onset and decreased the severity of lymphoproliferative disease in LAT knock-in mice. The pulmonary lymphocyte infiltration seen in LAT knock-in mice was also markedly decreased in double-mutant mice. Additionally, Erk activation was diminished in LAT knock-in Bam32 knockout CD4(+) T cells. To more accurately determine the role of Erk in this delay of lymphoproliferative disease, we also bred a transgenic, hypersensitive Erk allele (the Erk2 sevenmaker mutant) onto the LAT knock-in Bam32 knockout double-mutant background. These triple transgenic mice demonstrated a role for Erk activation in lymphoproliferative disease caused by the LAT knock-in mutation.
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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.