ArticleThe Journal of experimental medicine2002
Vav3 modulates B cell receptor responses by regulating phosphoinositide 3-kinase activation.
Article in The Journal of experimental medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 142 citations in OpenAlex.
- A molecular systems perspective on calcium oscillations beyond ion fluxes.Current opinion in cell biology · 2025Review
- Deciphering molecular mechanisms of SARS-CoV-2 pathogenesis and drug repurposing through GRN motifs: a comprehensive systems biology study.3 Biotech · 2023Article
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- BTK inhibitors in the treatment of hematological malignancies and inflammatory diseases: mechanisms and clinical studies.Journal of hematology & oncology · 2022Review
- Differential Requirement of Vav Proteins for Btk-dependent and -Independent Signaling During B Cell Development.Frontiers in cell and developmental biology · 2022Article
- Article
- Review
- The regulators of BCR signaling during B cell activation.Blood science (Baltimore, Md.) · 2019Review
- Review
- New insights into the Vav1 activation cycle in lymphocytes.Cellular signalling · 2018Article
- Role of Bruton's tyrosine kinase in B cells and malignancies.Molecular cancer · 2018Review
- A Novel Vav3 Homolog Identified in Lamprey, Lampetra japonica, with Roles in Lipopolysaccharide-Mediated Immune Response.International journal of molecular sciences · 2017Article
- The Calreticulin control of human stress erythropoiesis is impaired by JAK2V617F in polycythemia vera.Experimental hematology · 2017Article
- Grb2 carboxyl-terminal SH3 domain can bivalently associate with two ligands, in an SH3 dependent manner.Scientific reports · 2017Article
- Pathway Analysis of Genome-wide Association Study in Childhood Leukemia among Hispanics.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2016Article
- Ras-related C3 Botulinum Toxin Substrate (Rac) and Src Family Kinases (SFK) Are Proximal and Essential for Phosphatidylinositol 3-Kinase (PI3K) Activation in Natural Killer (NK) Cell-mediated Direct Cytotoxicity against Cryptococcus neoformans.The Journal of biological chemistry · 2016Article
- The multifaceted role of PIP2 in leukocyte biology.Cellular and molecular life sciences : CMLS · 2015Review
- The Function of Embryonic Stem Cell-expressed RAS (E-RAS), a Unique RAS Family Member, Correlates with Its Additional Motifs and Its Structural Properties.The Journal of biological chemistry · 2015Article
- Targeting Bruton's tyrosine kinase in B cell malignancies.Nature reviews. Cancer · 2014Review
- Vav family exchange factors: an integrated regulatory and functional view.Small GTPases · 2014Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To elucidate the mechanism(s) by which Vav3, a new member of the Vav family proteins, participates in B cell antigen receptor (BCR) signaling, we have generated a B cell line deficient in Vav3. Here we report that Vav3 influences phosphoinositide 3-kinase (PI3K) function through Rac1 in that phosphatidylinositol-3,4,5-trisphosphate (PIP3) generation was attenuated by loss of Vav3 or by expression of a dominant negative form of Rac1. The functional interaction between PI3K and Rac1 was also demonstrated by increased PI3K activity in the presence of GTP-bound Rac1. In addition, we show that defects of calcium mobilization and c-Jun NH2-terminal kinase (JNK) activation in Vav3-deficient cells are relieved by deletion of a PIP3 hydrolyzing enzyme, SH2 domain-containing inositol polyphosphate 5'-phosphatase (SHIP). Hence, our results suggest a role for Vav3 in regulating the B cell responses by promoting the sustained production of PIP3 and thereby calcium flux.
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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.