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Human VAV1 Protein expressed in HEK-293 Cells - ABIN2735197
Mahankali, Peng, Henkels, Dinauer, Gomez-Cambronero: Phospholipase D2 (PLD2) is a guanine nucleotide exchange factor (GEF) for the GTPase Rac2. in Proceedings of the National Academy of Sciences of the United States of America 2011
Study identifies the residues on EZH2 that are critical for its interaction with VAV and demonstrate that EZH2 interactions with VAV proteins are crucial for the regulation of adhesion dynamics and cellular transformation.
These results support a driver oncogenic role for VAV1 signaling in the pathogenesis of PTCL.
no significant association of FoxP3 promoter rs3761548 or (GT) n repeat length with presumed immunological graft failure. The genotype frequencies of Vav1 intron polymorphisms did not significantly differ between patients with graft failure and matched controls.
Data show that GEF Vav1 possesses tumor-suppressor functions in immature T cells.
Polymorphisms of VAV1 gene is associated with Rheumatoid arthritis.
Vav1 expression is increased in esophageal squamous cell carcinoma, indicates poor prognosis, and can serve as a candidate molecular prognostic marker.
TGFbeta induced the dissociation of DNMT1 from the VAV1 promoter, leading to demethylation and the subsequent ectopic expression of VAV1 in cancer cells via a SMAD4-dependent mechanism
Our results suggest the existence of a Vav1/PU.1/miR-142-3p network that supports all-trans retinoic acid -induced differentiation in acute promyelocytic leukemia -derived cells
revealed a new function for Vav1 in the negative feedback regulation of the phosphorylation of immunoreceptor tyrosine-based activation motifs within the zeta chains, CD3 delta, epsilon, gamma chains, as well as activation sites on the critical T cell tyrosine kinases
Data indicate that only a single mutation in the proto-oncogene Vav1 enhances tumorigenicity.
These findings establish VAV1 as a critical epigenetically regulated oncogene with a key role in MBSHH maintenance, and highlight its potential as a validated therapeutic target and prognostic biomarker for the improved therapy of medulloblastoma.
The present study implies that estrogen-estrogen receptor modulates the transcription and expression of Vav1, which may contribute to the proliferation of cancerous cells.
The role of Vav1 in T leukemia survival by selectively triggering Rac2-Akt axis and elevating the expression of anti-apoptotic Bcl-2.
results presented herein suggest a potential cross-talk between cancer cells and the microenvironment controlled by CSF1/Vav1 signaling pathways.
our data provide evidence that Vav1 is the linker molecule that couples CD28 to PIP5Kalpha activation and strongly fit with a potential model in which CD28 regulates PIP2 synthesis and turnover in T lymphocytes.
suggest that Vav1 promotes the matrix-degrading processes underlying tumor cell migration and further, under conditions of ectopic Vav1 expression, that Vav1 is a central regulator and major driver of invasive matrix remodeling by pancreatic tumor cells
VAV1 overexpression in both SKOV3 and human ovarian surface epithelial cells demonstrated that its upregulation of an E-cadherin transcriptional repressor, Snail and Slug, was not confined to ovarian cancer cells
The results highlight for the first time the potential role of Vav1 as an oncogenic stress activator in cancer and the p53 dependence of its pro-apoptotic effect in breast cells.
study provides evidence the large GTPase Dyn2 regulates the small GTPase Rac1 to potentiate invasive migration of pancreatic tumor cells; Dyn2 plays an essential role in regulating Rac1-mediated pancreatic tumor cell migration through modulation of the Rac1 activator Vav1 via a direct interaction
c-Abl tyrosine kinase plays a critical role in beta2 integrin-dependent neutrophil migration by regulating Vav1 activity.
the depletion of the micro RNA processing enzyme dicer in Vav1-positive cells allows interfering with post-yolk sac microglia recruitment
this study reveals a novel function of Vav1 in regulating mesenchymal stem cell fate decisions for differentiation through Sirt1.
Themis1 acts as a positive regulator of TCR signaling during thymocyte development by promoting Vav1 activity and Grb2 stability
Vav1 adaptor has a role in the production of inflammatory cytokines by effector T cells and in the susceptibility to neuroinflammation
provide evidence that CD28 and the TCR complex regulate NF-kappaB via different signaling modules of GRB-2/VAV1 and LAT/ADAP pathways respectively.
Platelet P-Rex and Vav family Rac-GEFs play important proinflammatory roles in leukocyte recruitment.
The data show that vav1 not only affects transcription of the MHCII locus but also is an important regulator of MHCII protein transport to the cell surface.
analyses revealed a SHP2- and Lyn-dependent pathway leading to phosphorylation of Vav1, Rac activation, and F-actin polymerization in SCF-treated BMMCs
Data indicate that Vav1 was a key negative regulator of macrophage-derived IL-6 production.
Bruton's Tyrosine Kinase (BTK) and Vav1 contribute to Dectin1-dependent phagocytosis of Candida albicans in macrophages.
Suggest that Vav1 act as critical molecular link coupling hyperlipidemia with proatherogenic monocyte/macrophage responses.
Loss of Vav1 activity does not favour development of colitis-associated colon cancer.
SH2 and SH3(B) domains of Vav1 are critical for the phosphorylation of Vav1 and its signalling function in TCR-induced calcium flux.
SAP couples SLAM family receptors to the kinase Fyn, which triggered the exchange factor Vav-1 and augmented NK cell activation.
the GDP exchange factor activity is required for T cell mediated allograft rejection
The oncogenic truncation of this region elicits conformational changes that interfere with the Vav1-mediated activation of PLCgamma1 and that inhibit calcium mobilization.
Dectin-1 activates the integrin Mac-1 in neutrophils via Vav1 and Vav3 signaling to promote Candida albicans clearance.
identified previously unknown components of the CD36 signaling pathway, demonstrating that Vav proteins regulate oxLDL uptake and foam cell formation via calcium- and dynamin 2-dependent processes
Data show that abnormal perivascular localization correlated with decreased retention of Vav1(-/-) HSPC in the bone marrow (44-60% reduction at 48 h posttransplant.
This gene is a member of the VAV gene family. The VAV proteins are guanine nucleotide exchange factors (GEFs) for Rho family GTPases that activate pathways leading to actin cytoskeletal rearrangements and transcriptional alterations. The encoded protein is important in hematopoiesis, playing a role in T-cell and B-cell development and activation. The encoded protein has been identified as the specific binding partner of Nef proteins from HIV-1. Coexpression and binding of these partners initiates profound morphological changes, cytoskeletal rearrangements and the JNK/SAPK signaling cascade, leading to increased levels of viral transcription and replication. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
vav 1 oncogene
, proto-oncogene vav
, vav oncogene