ArticleSmall GTPases2011
Ca-dependent Ras/Erk signaling mediates negative selection of autoreactive B cells.
Article in Small GTPases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- DYRK1A inhibition results in MYC and ERK activation rendering KMT2A-R acute lymphoblastic leukemia cells sensitive to BCL2 inhibition.Leukemia · 2025Article
- FCRL1 Regulates B Cell Receptor-Induced ERK Activation through GRB2.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Endoplasmic reticulum & mitochondrial calcium homeostasis: The interplay with viruses.Mitochondrion · 2021Article
- Signaling mechanisms regulating B-lymphocyte activation and tolerance.Journal of molecular medicine (Berlin, Germany) · 2015Review
- Activation of Ras overcomes B-cell tolerance to promote differentiation of autoreactive B cells and production of autoantibodies.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Targeting the B-cell receptor signaling pathway in B lymphoid malignancies.Current opinion in hematology · 2014Review
- Protein kinase Cδ promotes transitional B cell-negative selection and limits proximal B cell receptor signaling to enforce tolerance.Molecular and cellular biology · 2014Article
- Elements of the B cell signalosome are differentially affected by mercury intoxication.Autoimmune diseases · 2014Article
- The expanding spectrum of the autoimmune lymphoproliferative syndromes.Current opinion in pediatrics · 2013Review
- RasGRP Ras guanine nucleotide exchange factors in cancer.Frontiers in biology · 2013Article
- Regulation of ras exchange factors and cellular localization of ras activation by lipid messengers in T cells.Frontiers in immunology · 2013Review
- Loss-of-function of the protein kinase C δ (PKCδ) causes a B-cell lymphoproliferative syndrome in humans.Blood · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signaling via the Ras/Erk pathway has long been recognized to be critical in lymphocyte development and function, yet the mechanisms that control the distinct functional outputs of this pathway in different cellular contexts remain poorly understood. Our recent results have demonstrated unexpected involvement of Ras/Erk signaling in the sensitization of B cells to apoptosis in order to eliminate autoreactive cells. Increases in cytosolic Ca(2+) are necessary and sufficient to induce activation of this Ras/Erk pathway, and the biochemical events involved in its activation are different from the ones involved in diacylglycerol (DAG)-mediated Ras/Erk activation. Developmental regulation of upstream mediators of these distinct pathways contributes to their predominant activation at different stages of B cell development. These findings have revealed a mechanism by which antigen stimulation can activate distinct Ras/Erk pathways at different developmental stages to mediate appropriate functional outputs that control the selection, development and activation of B cells. Despite these recent findings, however, much remains to be learned about the molecular mechanisms that confer functional specificity to common Ras/Erk signaling modules.
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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.