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Proto-Oncogene Proteins c-vavGuanine Nucleotide Exchange FactorsOncogene ProteinsCell Cycle Proteinsrac1 GTP-Binding ProteinProto-Oncogene Proteinsrac GTP-Binding ProteinsJurkat CellsSignal TransductionReceptors, Antigen, T-CellPhosphorylationTyrosinePhospholipase C gammacdc42 GTP-Binding Proteinsrc Homology Domainsrho GTP-Binding ProteinsNFATC Transcription FactorsZAP-70 Protein-Tyrosine KinaseAdaptor Proteins, Signal TransducingT-LymphocytesSOS1 Proteinrho Guanine Nucleotide Dissociation Inhibitor betaHydrophthalmosProtein-Tyrosine KinasesSon of Sevenless ProteinsGRB2 Adaptor ProteinrhoA GTP-Binding ProteinEnzyme ActivationPhosphotyrosinePhosphoproteinsProtein BindingReceptors, Antigen, B-Cellras Guanine Nucleotide Exchange FactorsMice, KnockoutTransfection3T3 CellsKymographyOncogene Protein v-cblp21-Activated KinasesCell LineCytoskeletonProtein Structure, TertiaryEphrin-A1Muromonab-CD3Heterogeneous-Nuclear Ribonucleoprotein KRecombinant Fusion ProteinsPhosphatidylinositol 3-KinasesProto-OncogenesAntigens, CD28ActinsJNK Mitogen-Activated Protein KinasesType C PhospholipasesMitogen-Activated Protein KinasesLymphocyte ActivationProteinsCOS CellsEnzyme Precursorssrc-Family KinasesHematopoietic SystemMolecular Sequence DataPseudopodiaProto-Oncogene Proteins c-fynrho-Specific Guanine Nucleotide Dissociation InhibitorsProto-Oncogene Proteins c-cblB-LymphocytesGene Expression RegulationIntracellular Signaling Peptides and ProteinsLymphocyte Specific Protein Tyrosine Kinase p56(lck)Amino Acid SequenceDynamin IIImmunoprecipitationNuclear ProteinsCell MovementReceptor, EphA2Cells, CulturedGTP PhosphohydrolasesPrecipitin TestsMutationAdaptor Proteins, Vesicular TransportGuanine Nucleotide Dissociation InhibitorsRetroviridae Proteins, OncogenicGuanosine DiphosphateDNA-Binding ProteinsInterleukin-2Cell AdhesionIntegrinsReceptor-CD3 Complex, Antigen, T-CellReceptors, IgETwo-Hybrid System TechniquesCalcium-Calmodulin-Dependent Protein KinasesCell Surface ExtensionsPhosphatidylinositol PhosphatesTranscription FactorsAntigens, CD18Antigens, CD19Immunological SynapsesAntiveninsRho Guanine Nucleotide Exchange FactorsBinding SitesCell Line, Tumor
VAV1VAV3GuanineInteractionProteinsGrb2ReceptorCellResponseFamilyVav3RhoAPhosphorylationHypothesisStimulationActivationShownExpressionFact
VAV19
  • Unlike VAV1, which is expressed exclusively in hematopoietic cells, VAV2 transcripts were found in most tissues. (wikipedia.org)
  • Furthermore, we found a similar novel phenotype in the absence of Vav1, Vav2, and Vav3, which function as guanine nucleotide exchange factors for Rac1 and Rac2. (northwestern.edu)
  • Vav1, Vav2, and Vav3 Vav proteins had been first referred to as proto-oncogenes performing as substrates for tyrosine protein kinase activity (33). (neighborhoodhousecharterschool.org)
  • Latest studies analyzing the part of Vav family members proteins, including Vav1, Vav2, and Vav3, in lymphocytes possess revealed their important function to hyperlink lymphocyte antigen receptor activation to actin cytoskeleton dynamics. (neighborhoodhousecharterschool.org)
  • Vav1, Vav2, and Vav3 talk about a lot more than 50% homology in the protein sequences, which are composed of the Dbl-homologous (DH) site, pleckstrin homology (PH) site, SH2/SH3 site, proline rich region, and a calponin homology (CH) site (34). (neighborhoodhousecharterschool.org)
  • Vav1 can be indicated in every haematopoietic cells extremely, whereas Vav2 displays the highest manifestation in splenic adult B cells in comparison with additional B cell subsets, recommending an important part of Vav2 in adult B cell homeostasis. (neighborhoodhousecharterschool.org)
  • All three PF-04937319 proteins of Vav1, Vav2, and Vav3 are phosphorylated following the antigen receptor engagement quickly. (neighborhoodhousecharterschool.org)
  • solitary knockout mice, Vav1, Vav2, and Vav3 may have functional redundancy downstream of BCR activation. (neighborhoodhousecharterschool.org)
  • Contrastingly, Vav1 expression was not detected while low levels of Vav2 expression were detected. (medicineinnovates.com)
VAV32
  • The recruitement of VAV2, VAV3 and PI3-kinase p85 subunit by phosphorylated EPHA2 is critical for EFNA1-induced RAC1 GTPase activation and vascular endothelial cell migration and assembly (By similarity). (abcam.com)
  • Although Vav2 and Vav3-alpha expression in cancers was independently distributed with regard to the degree of platinum responsiveness, Vav3.1 was expressed at significantly higher levels in platinum-refractory cancers compared to all other cancers. (medicineinnovates.com)
Guanine1
  • Guanine nucleotide exchange factor VAV2 is a protein that in humans is encoded by the VAV2 gene. (wikipedia.org)
Interaction1
Proteins1
  • We identified five proteins, Hrs, Vav2, c-Kit, the regulatory subunit of Pi3k (P85), and Fgfr1, that were over- or under-phosphorylated in the mutant lung, suggesting that they could be indispensable effectors of the TGF-β signaling program during embryonic lung development. (nih.gov)
Grb21
  • VAV2 has been shown to interact with CD19 and Grb2. (wikipedia.org)
Receptor1
  • We observed that direct stimulation with LT D4, induced intestinal epithelial cell migration, through activation of the CysLT1 receptor, phosphotidylinositol-3 kinase, Vav2 and Rac localisation to membrane ruffles. (lu.se)
Cell2
  • These data define a novel pathway that directs Lyn/Src family tyrosine kinase signals to sarcoma cell invadopodia through specific recruitment of Vav2 and Nck2 to phosphorylated AFAP1L1, to control cell migration and invasion. (nature.com)
  • Because T cell function and subsets are suggested to become unaltered in Vav2? (neighborhoodhousecharterschool.org)
Response3
Family1
  • VAV2 is the second member of the VAV oncogene family. (wikipedia.org)
Vav32
  • Corrigendum: Association of VAV2 and VAV3 polymorphisms with cardiovascular risk factors. (nih.gov)
  • EphA4 activation leads autophosphorylation of Tyr-596 and Tyr-602, and the conserved sites in EphA2 are required for binding to the GEFs, Vav2 and Vav3, and ephrin-induced cell migration. (ecmbio.com)
RhoA3
  • Tyrosine-Phosphorylated Caveolin-1 Blocks Bacterial Uptake by Inducing Vav2-RhoA-Mediated Cytoskeletal Rearrangements. (mpg.de)
  • Respondent falsified Figure 5 from NIGMS, NIH, grant application GM047607-18A1, by falsifying Western blot data to support the hypothesis that co-transfection of PKL plus RhoA GEF Vav2 induces RhoA activation and signaling upon plating on fibronectin. (nih.gov)
  • Rather, phosphorylated Vav2 showed related tendency to bind both Rac and RhoA. (trpv1inhibitor.com)
Phosphorylation3
  • The kinase is activated by prolactin stimulation, leading to phosphorylation of VAV2 guanine nucleotide exchange factor, paxillin, and activation of the RAC1 GTPase. (nih.gov)
  • Contributes to prolactin-mediated phosphorylation of PXN and VAV2. (nih.gov)
  • Implicated in prolactin-mediated cytoskeletal reorganization and motility of breast cancer cells through mechanisms involving RAC1 activation and phosphorylation of PXN and VAV2. (nih.gov)
Hypothesis1
  • Inhibition of DHFR by 6 and 7 confirms VAV2 our hypothesis the fact that substitution of the 2-methyl group by 2-amino group in benzo[4,5]thieno[2,3-with a rotary evaporator. (bio-biz-navi.com)
Stimulation1
  • Its been demonstarted that L1 stimulation propagates through VAV2-Rac1-Pak1 to MEK-ERK. (reactome.org)
Activation1
  • Scholars@Duke publication: Potentially functional genetic variants of VAV2 and PSMA4 in the immune-activation pathway and non-small cell lung cancer survival. (duke.edu)
Shown1
  • The most active R&D compound to date (see Figure 3) is Vav2, which has been shown by this application to be non-selective and HBT does not block any of its effects. (takepharmacologyexam.com)
Expression1
  • Respondent falsified Figure 3I in a manuscript submitted for publication to the Journal of Cell Biology by falsely labeling a Western blot to indicate levels of expression for various Vav2 mutants, when the experimental data were taken from a completely unrelated experiment. (nih.gov)
Fact1
  • Respondent falsified Figure 1A in a manuscript submitted for publication to the Journal of Cell Biology , by altering immunoprecipitation Western blot data to make this experiment appear that no Vav2 SH2 was associated with PKL 3YF, when in fact it did. (nih.gov)