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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.
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These results support a driver oncogenic role for VAV1 signaling in the pathogenesis of PTCL.
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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.
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Data show that GEF Vav1 possesses tumor-suppressor functions in immature T cells.
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Polymorphisms of VAV1 gene is associated with Rheumatoid arthritis.
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Vav1 expression is increased in esophageal squamous cell carcinoma, indicates poor prognosis, and can serve as a candidate molecular prognostic marker.
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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
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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
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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
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Data indicate that only a single mutation in the proto-oncogene Vav1 enhances tumorigenicity.
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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.
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The present study implies that estrogen-estrogen receptor modulates the transcription and expression of Vav1, which may contribute to the proliferation of cancerous cells.
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The role of Vav1 in T leukemia survival by selectively triggering Rac2-Akt axis and elevating the expression of anti-apoptotic Bcl-2.
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results presented herein suggest a potential cross-talk between cancer cells and the microenvironment controlled by CSF1/Vav1 signaling pathways.
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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.
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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
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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
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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.
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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
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c-Abl tyrosine kinase plays a critical role in beta2 integrin-dependent neutrophil migration by regulating Vav1 activity.
