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anti-Rat (Rattus) WASF2 Anticorps:
anti-Human WASF2 Anticorps:
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Bat Polyclonal WASF2 Primary Antibody pour WB - ABIN6746329
Frain, Swart, Monaci, Nicosia, Stämpfli, Frank, Cortese: The liver-specific transcription factor LF-B1 contains a highly diverged homeobox DNA binding domain. dans Cell 1989
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Human Polyclonal WASF2 Primary Antibody pour ELISA, WB - ABIN548436
Suetsugu, Tanaka: Crystal growth of carbonate apatite using a CaCO3 flux. dans Journal of materials science. Materials in medicine 2004
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High WAVE2 expression in pancreatic cancer tissues was correlated with overall survival. WAVE2 accumulated in the cell protrusions of pancreatic cancer cell lines through ACTN4 recruitment to filamentous actin in the protrusions and the activation of p27, resulting in an increase in motility and invasiveness of pancreatic ductal adenocarcinoma cells.
Results show that in cisplatin-resistant cervical cancer tissues, Rac1, and Wave2 mRNA expression was significantly up-regulated compared to that of the cisplatin-sensitive cervical cancer tissues. In HeLa and Caski cervical cancer cell lines, Rac1 activity and Wave2 protein expression was significantly promoted by SH3BP1 overexpression.
Studied leucine rich repeat kinase 2 (LRRK2)-WAS protein family member 2 (WAVE2) pathway in modulation of phagocytosis in leukocytes, as well as its possible role for altered immune function in Parkinson's Disease.
The level of WASF2 in gastric cancer tissues was negatively correlated with miR-146a expression and had inverse clinicopathologic features. The newly identified miR-146a/WASF2 axis may provide a novel therapeutic target for gastric cancer.
These findings indicate that inhibition of the Rac1WAVE2Arp2/3 signaling pathway may promote radiosensitivity, which may partially result from the downregulation of CFL1 in U251 human glioma cells.
SH3BP1 promoted VEGF secretion via Rac1-WAVE2 signaling, so as to exert an augmentation on cell invasion and microvessel formation.
the MCP1-induced cortactin phosphorylation is dependent on PLCb3-mediated PKC activation, and siRNA-mediated down-regulation of either of these molecules prevents cortactin interaction with WAVE2
WASp and WAVE2 differ in their dynamics and their associated proteins
Decreased expression of Wiskott-Aldrich syndrome protein family verprolin-homologous protein 2 may be involved in the development of pre-eclampsia.
these results suggest that Arp2/3 and the upstream regulator, WAVE2, are essential co-factors hijacked by HIV for intracellular migration, and may serve as novel targets to prevent HIV transmission.
WAVE2 is down-regulated in gastric cancer
Cortactin has a role as a scaffold for Arp2/3 and WAVE2 at the epithelial zonula adherens
data reveal a critical role for WAVE2 complex in regulation of cellular signaling and epithelial morphogenesis
Identification of an onco-suppressive role of miR-146a in gastric cancer cells by its reduction of WASF2 expression.
We demonstrate that WAVE2-Arp2/3 is a major nucleator of actin assembly at the zonula adherens and likely acts in response to junctional Rac signaling
results suggest that SKAP2 negatively regulates cell migration and tumor invasion in fibroblasts and glioblastoma cells by suppressing actin assembly induced by the WAVE2-cortactin complex
results indicate that by mediating intensive F-actin accumulation at the sites of cell infiltration, WAVE2, N-WASP, and Mena are crucial for PI3K-dependent cell invasion induced by PDGF
WAVE2 and WASp define parallel pathways to F-actin reorganization and function in NK cells; although WAVE2 was not required for NK cell innate function, it was accessible through adaptive immunity via IL-2.
Data suggest that ERK coordinates adhesion disassembly with WAVE2 regulatory complex activation and actin polymerization to promote productive leading edge advancement during cell migration.
WAVE2 works as an A-kinase-anchoring protein that recruits PKA at membrane protrusions and plays a role in the enlargement of membrane protrusions induced by PKA activation
WAVE2/c-Abl survival signal required at the hematopoietic stem cell (HSC) fetal liver to marrow transition that confers fitness to the HSC for marrow hematopoiesis
TrkC signals to the podocyte actin cytoskeleton to induce migration by phosphorylating WAVE2 Erk dependently. This signaling mechanism may be important for TrkC-mediated cytoskeletal dynamics in podocyte disease.
Rho family GTPases use the I-BAR proteins, IRSp53 (also known as BAIAP2), IRTKS and Pinkbar, as a central mechanism to modulate cell morphology.
Data show that the primary effect of costimulation blockade was to decrease recruitment of the activator of actin nucleation WAVE2 (Wiskott-Aldrich syndrome protein family member protein 2) and cofilin (actin-severing protein) to F-actin.
The expression of NESH/Abi-3 caused degradation of endogenous Abi-1, which led to the formation of a NESH/Abi-3-based WAVE2 complex.
This study demonstrated that WAVE2-Abi2 complex, which controls growth cone activity, is crucial for completing transition from a multipolar to bipolar shape.
Results of the present study show that the nucleation-promoting factors JMY and WAVE2 are critical for cytokinesis during development of mouse embryos.
These results identify Wasf2 as a novel target of intermittent PTH administration via the Wnt and phosphoinositide-dependent protein kinase signaling pathways.
The protein and messenger RNA levels of WAVE2 were decreased in aged oocytes, but the levels were normal in caffeine-treated aged oocytes.
mDia1 and WAVE2 are important Src homology 3 domain partners of IRSp53 in forming filopodia.
WAVE2 regulates oocyte polarization by regulating meiotic spindle, peripheral positioning, probably via an actin-mediated pathway, and is involved in polar body emission during mouse oocyte meiotic maturation.
sential role for Abi1 in embryonic survival and WAVE2 complex integrity
Scar2 and the Arp2/3 complex appear to be involved in the establishment and maintenance of Golgi polarity during directed migration
WAVE2 colocalised with IRSp53 at the tips of protruding lamellipodia and filopodia, and the IRSp53 signal in filopodia decreased before that of WAVE2 during retraction.
WAVE2 deficiency reveals distinct roles in embryogenesis and Rac-mediated actin-based motility.
WAVE2-regulated actin reorganization might be required for proper cell movement and that a lack of functional WAVE2 impairs angiogenesis in vivo
Results suggest that phosphatidylinositol (3,4,5)-triphosphate recruits WAVE2 to the polarized membrane and that this recruitment is essential for lamellipodium formation at the leading edge.
results imply that both N-WASP and WAVE2 proteins, which are activated downstream of phosphati-dylinositol 3-kinase, are required for the migration through the lamellipodial formation of myocyte C2C12 cells induced by hepatocyte growth factor
WAVE2 acts as the primary effector downstream of Rac to achieve invasion and metastasis, suggesting that suppression of WAVE2 activity holds a promise for preventing cancer invasion and metastasis.
This gene encodes a member of the Wiskott-Aldrich syndrome protein family. The gene product is a protein that forms a multiprotein complex that links receptor kinases and actin. Binding to actin occurs through a C-terminal verprolin homology domain in all family members. The multiprotein complex serves to tranduce signals that involve changes in cell shape, motility or function. The published map location (PMID:10381382) has been changed based on recent genomic sequence comparisons, which indicate that the expressed gene is located on chromosome 1, and a pseudogene may be located on chromosome X. Two transcript variants encoding different isoforms have been found for this gene.
WAS protein family, member 2
, wiskott-Aldrich syndrome protein family member 2
, WASP family Verprolin-homologous protein 2
, WASP family protein member 2
, WASP family protein member 4
, protein WAVE-2
, putative Wiskott-Aldrich syndrome protein family member 4
, suppressor of cyclic-AMP receptor (WASP-family)
, verprolin homology domain-containing protein 2