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抗Human VAV1 抗体:
抗Rat (Rattus) VAV1 抗体:
抗Mouse (Murine) VAV1 抗体:
Human Polyclonal VAV1 Primary Antibody for IHC - ABIN967242
Amarasinghe, Rosen: Acidic region tyrosines provide access points for allosteric activation of the autoinhibited Vav1 Dbl homology domain. in Biochemistry 2005
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Human VAV1 Primary Antibody for WB - ABIN967241
Charvet, Canonigo, Billadeau, Altman: Membrane localization and function of Vav3 in T cells depend on its association with the adapter SLP-76. in The Journal of biological chemistry 2005
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Human Monoclonal VAV1 Primary Antibody for FACS, ELISA - ABIN969581
Bertagnolo, Nika, Brugnoli, Bonora, Grassilli, Pinton, Capitani: Vav1 is a crucial molecule in monocytic/macrophagic differentiation of myeloid leukemia-derived cells. in Cell and tissue research 2011
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Human Polyclonal VAV1 Primary Antibody for WB - ABIN362132
Sekine, Ikeda, Tsuji, Yamamoto, Muromoto, Nanbo, Oritani, Yoshimura, Matsuda: Signal-transducing adaptor protein-2 regulates stromal cell-derived factor-1 alpha-induced chemotaxis in T cells. in Journal of immunology (Baltimore, Md. : 1950) 2009
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 (显示 TGFB1 抗体) induced the dissociation of DNMT1 (显示 DNMT1 抗体) from the VAV1 promoter, leading to demethylation and the subsequent ectopic expression of VAV1 in cancer cells via a SMAD4 (显示 SMAD4 抗体)-dependent mechanism
Our results suggest the existence of a Vav1/PU.1/miR (显示 MLXIP 抗体)-142-3p network that supports all-trans retinoic acid -induced differentiation in acute promyelocytic leukemia (显示 PML 抗体) -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 (显示 CD3D 抗体), 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 (显示 RAB1A 抗体) Vav1 enhances tumorigenicity.
These findings establish VAV1 as a critical epigenetically regulated oncogene (显示 RAB1A 抗体) 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 (显示 ESR1 抗体) 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 (显示 RAC2 抗体)-Akt (显示 AKT1 抗体) axis and elevating the expression of anti-apoptotic Bcl-2 (显示 BCL2 抗体).
results presented herein suggest a potential cross-talk between cancer cells and the microenvironment controlled by CSF1 (显示 CSF1 抗体)/Vav1 signaling pathways.
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 (显示 CD28 抗体) and the TCR complex regulate NF-kappaB (显示 NFKB1 抗体) via different signaling modules of GRB-2 (显示 GRB2 抗体)/VAV1 and LAT (显示 LAT 抗体)/ADAP (显示 APP 抗体) pathways respectively.
Platelet P-Rex and Vav family Rac (显示 AKT1 抗体)-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 (显示 PTPN11 抗体)- and Lyn (显示 LYN 抗体)-dependent pathway leading to phosphorylation of Vav1, Rac (显示 AKT1 抗体) activation, and F-actin polymerization in SCF (显示 KITLG 抗体)-treated BMMCs
Data indicate that Vav1 was a key negative regulator of macrophage-derived IL-6 (显示 IL6 抗体) production.
Bruton's Tyrosine Kinase (BTK (显示 BTK 抗体)) and Vav1 contribute to Dectin1 (显示 CLEC7A 抗体)-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.
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