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anti-Human VAV2 Antikörper:
anti-Rat (Rattus) VAV2 Antikörper:
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Human Polyclonal VAV2 Primary Antibody für ELISA, WB - ABIN257860
Henske, Short, Jozwiak, Bovey, Ramlakhan, Haines, Kwiatkowski: Identification of VAV2 on 9q34 and its exclusion as the tuberous sclerosis gene TSC1. in Annals of human genetics 1995
Human Polyclonal VAV2 Primary Antibody für IHC, IHC (p) - ABIN4364881
Zhu, Zhao, Wu, Yang, Shao, Wang, Wu, Yin, Li, Hou, Zhang, Zhou, Gu, Wang, Bustelo, Zhou: Identification of a Vav2-dependent mechanism for GDNF/Ret control of mesolimbic DAT trafficking. in Nature neuroscience 2015
Both erb-b2 receptor tyrosine kinase 2 (ErbB2) and vav guanine nucleotide exchange factor 2 (VAV2 )are direct targets of miR-331-3p.
VAV2 polymorphisms associate with cardiovascular risk factors and target organ damage.
Study found that Vav2, is overexpressed in human prostate cancer and enhanced AR and AR splicing variant activity.
High VAV2 expression is associated with breast cancer.
Manipulating steroidogenic factor-1 (SF-1) and nucleotide exchange factor VAV-2 (VAV2) abundance in cultured adrenocortical carcinoma (ACC) cells indicate that VAV2 was a critical factor for SF-1-induced cytoskeletal remodeling and invasion in culture and in vivo (chicken chorioallantoic membrane) models.
Data indicate that phosphorylated cortactin recruits Vav2 to activate Rac3 and promote invadopodial maturation in invasive breast cancer cells.
autocrine VEGF and IL-8 promoted endothelial cell migration via the Src/Vav2/Rac1/PAK1 signaling pathway.
We concluded that Vav2 might promote invasion and metastasis of gastric cancer by regulating some invasion and metastasis-related genes.
work suggested that EphB3 acted as a tumor promoter in Papillary Thyroid Cancer by increasing the in vitro migration as well as the in vivo metastasis of Papillary Thyroid Cancer cells through regulating the activities of Vav2 and Rho GTPases in a kinase-dependent manner.
The crystal structure of the complex between a phosphorylated PPxY motif of TXNIP and the SH2 domain of Vav2 reveals a conserved recognition mechanism.
Our data provide the first evidence to implicate VAV2 in glucose-induced Rac1 activation, actin remodelling and glucose-stimulated insulin secretion in pancreatic beta cells.
VAV2 is required for Met signaling in the perinuclear endosome.
Authors propose a model whereby vimentin promotes FAK stabilization through VAV2-mediated Rac1 activation. This model may explain why vimentin expressing metastatic lung cancer cells are more motile and invasive.
Data suggest a coordination between paxillin kinase linker (PKL)/Vav2 signaling and PKL/beta-PIX signaling during cell migration.
the guanine nucleotide exchange factor (GEF) Vav2 is identified as a candidate partner for KCC3.
Two variants of VAV2 and VAV3, rs2156323 and rs2801219, respectively, were identified in Japanese patients with primary open angle glaucoma, normal tension glaucoma, and developmental glaucoma.
Upregulation of Rac1 activity by Wnt3a temporally correlated with enhanced p120-catenin binding to Rac1 and Vav2.
Studies indicate relevance of P-Rex1 and P-Rex2a, in breast tumorigenesis, and suggest that the exchange factors Vav2 and Vav3 play synergistic roles in breast cancer by sustaining tumor growth, neoangiogenesis, and metastasis.
Data indicate that Vav2 and Vav3 controlled a vast transcriptional program in breast cancer cells through mechanisms that were shared between the two proteins, isoform-specific or synergistic.
The structural basis for the interaction between Arap3 and Vav2, hydrophobic pockets and binding specificity.
reduction of VAV2 in absence of CUX1 was associated with a significant decrease of RAC1 activity in response to epithelial wounding. Our results identify a novel pathway by which CUX1 regulates normal intestinal epithelial cell restitution
This inhibitory action of Vav2 shRNA on Hcys-induced podocyte injury was associated with reduction of Rac1 activity and ROS production. These results suggest that elevated Hcys levels activate Vav2 and thereby increase NOX activity leading to ROS production, which triggers NLRP3 inflammasome activation, podocyte dysfunction and glomerular injury.
Results show that Vav2 and Rac1 are commonly involved in blood pressure regulation.
Data demonstrate that the co-expression of the exchange factors Vav2 and Vav3 is critical for the development of this tumor type.
Vav2 and Vav3 are required for normal peripheral nerve degeneration/regeneration, revascularization and functional recovery.
The results indicate that ADIP plays an essential role in PDGF-induced cell movement by interacting with afadin and Vav2 and regulating the activation of Rac.
CD36 contributes to activation of Vav-1, -2, and -3 in aortae from hyperlipidemic mice
Cbl ubiquitin ligase plays a critical role in the maintenance of AJs and suppression of cell migration through down-regulation of EGFR-Vav2 signaling.
Data show that Vav2/Vav3-deficient mice show early onset of iridocorneal angle changes and elevated intraocular pressure, with subsequent selective loss of retinal ganglion cells and optic nerve head cupping, which are the hallmarks of glaucoma.
Vav2 controls nitric oxide-dependent responses in mouse vascular smooth muscle cells.
does not contribute to platelet aggregation by CRP and thrombin, and is not required for regulation of phospholipase C.
Vav2 and Tiam1 may act as downstream effectors of Src, thereby regulating Rac1-dependent pathways that participate in Src-induced cell transformation
Three Vav proteins (vav1,vav2 and vav3) function specifically in distinct pathways that trigger NK cell cytotoxicity.
Vav2 is a GEF responsible for the nectin-induced, c-Src-, and Cdc42-mediated activation of Rac
Vav proteins regulate an NF-kappaB-dependent survival signal in naive B cells and are required for NF-kappaB function after BCR cross-linking
Vav2-deficient macrophages display a high level of constitutive membrane ruffling.
The viral protein M2 may have a role in disseminating the latent virus by modulating B-cell receptor-mediated signaling events through Vav1 and Vav2 to promote B-cell activation, proliferation, and survival.
This study showed that Vav1 and Vav3 are required for optimal spreading and regulation of PLCgamma2 by integrin alphaIIbbeta3, but that their requirement is by-passed upon G-protein receptor activation.
These results indicate that Vav2 plays crucial roles in the maintenance of cardiovascular homeostasis in mice.
role of Vav1 and Vav2 in allogeneic T-cell activation, antibody responses and allograft rejection
VAV2 is the second member of the VAV guanine nucleotide exchange factor family of oncogenes. Unlike VAV1, which is expressed exclusively in hematopoietic cells, VAV2 transcripts were found in most tissues. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
guanine nucleotide exchange factor VAV2
, vav 2 oncogene
, Vav2 oncogene