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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Wiskott-Aldrich syndrome

Wasp, Wiskott-Aldrich syndrome protein
The Wiskott-Aldrich syndrome (WAS) family of proteins share similar domain structure, and are involved in transduction of signals from receptors on the cell surface to the actin cytoskeleton. The presence of a number of different motifs suggests that they are regulated by a number of different stimuli, and interact with multiple proteins. Recent studies have demonstrated that these proteins, directly or indirectly, associate with the small GTPase, Cdc42, known to regulate formation of actin filaments, and the cytoskeletal organizing complex, Arp2/3. Wiskott-Aldrich syndrome is a rare, inherited, X-linked, recessive disease characterized by immune dysregulation and microthrombocytopenia, and is caused by mutations in the WAS gene. The WAS gene product is a cytoplasmic protein, expressed exclusively in hematopoietic cells, which show signalling and cytoskeletal abnormalities in WAS patients. A transcript variant arising as a result of alternative promoter usage, and containing a different 5' UTR sequence, has been described, however, its full-length nature is not known. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Actin, N-WASP, Arp2, CAN, Cdc42
Papers using Wasp antibodies
Phosphoinositide regulation of the actin cytoskeleton
Yin Helen L. et al., In The Journal of Cell Biology, 2002
... ); anti–PIP5K-α, -RhoA, -ERK, -Syk, -myc, -WASP, and -pY (Santa Cruz Biotechnology, Inc.); anti–active WASP (a ...
Formation of filopodia-like bundles in vitro from a dendritic network
Borisy Gary G. et al., In The Journal of Cell Biology, 2000
... Met, Arg, Gly, Ser (MRGS) 6xHis and FLAG epitopes was amplified by PCR from a human WASP cDNA (a gift of Arie Abo, PPD Discovery, Menlo Park, ...
The Intersectin 2 Adaptor Links Wiskott Aldrich Syndrome Protein (WASp)-mediated Actin Polymerization to T Cell Antigen Receptor Endocytosis
Siminovitch Katherine A. et al., In The Journal of Experimental Medicine, 1999
... For the two hybrid screen, the full-length human WASP cDNA was subcloned into the pAS1 vector and the resulting construct transfected into yeast cells harboring the MATCHMAKER activated human T cell DNA library in the pGAD10 vector (CLONTECH Laboratories, Inc.) ...
Papers on Wasp
Invadopodia proteins, cortactin, N-WASP and WIP differentially promote local invasiveness in ameloblastoma.
Ng et al., Kuala Lumpur, Malaysia. In J Oral Pathol Med, Feb 2016
N-WASP, which coordinates actin polymerization and invadopodia-mediated extracellular matrix degradation, was overexpressed in the solid/multicystic subtype (P < 0.05).
A Sensitized Screen for Genes Promoting Invadopodia Function In Vivo: CDC-42 and Rab GDI-1 Direct Distinct Aspects of Invadopodia Formation.
Sherwood et al., Boston, United States. In Plos Genet, Jan 2016
CDC-42 is required for the invasive membrane localization of WSP-1 (N-WASP), a CDC-42 effector that promotes polymerization of F-actin.
An Insulin-binding Protein from the Venom of a Solitary Wasp Eumenes pomiformis Binds to Apolipophorin III in Lepidopteran Hemolymph.
Kim et al., Chinju, South Korea. In Toxicon, Jan 2016
UNASSIGNED: EpIBP, an insulin-like peptide-binding protein, is a major protein component of the venom of a solitary hunting wasp, Eumenes pomiformis.
Decreased expression of cortactin in the schizophrenia brain.
Meador-Woodruff et al., New York City, United States. In Neuroreport, Jan 2016
To determine whether the Arp2/3 complex is abnormally expressed in schizophrenia, we measured the protein expression of Arp2 and Arp3, as well as Arp2/3 complex binding partners and associated proteins including cortactin, neuronal-Wiskott-Aldrich syndrome protein (WASP), WASP-family verprolin homologous protein 1 (WAVE1), and Abelson interactor 1 (Abi1) in the superior temporal gyrus of paired schizophrenia and comparison participants.
Differential Genomic Effects on Signaling Pathways by Two Different CeO2 Nanoparticles in HepG2 Cells.
Kitchin et al., In J Nanosci Nanotechnol, Dec 2015
M is more active than L in respect to altering the pathways of mitochondrial dysfunction, acute phase response, apoptosis, 14-3-3 mediated signaling, remodeling of epithelial adherens junction signaling, actin nucleation by ARP-WASP complex, altered TCA cycle and elevated fatty acid concentrations by metabolomics.
The WASP-WIP complex in the molecular pathogenesis of Wiskott-Aldrich syndrome.
Sasahara, Japan. In Pediatr Int, Oct 2015
The gene responsible for X-linked WAS encodes the Wiskott-Aldrich syndrome protein (WASP), which is expressed in hematopoietic cells and which regulates T cell activation and cytoskeletal reorganization in T cell receptor (TCR) signaling.
APP intracellular domain-WAVE1 pathway reduces amyloid-β production.
Kim et al., New York City, United States. In Nat Med, Sep 2015
Here we report that the amyloid precursor protein (APP) intracellular domain (AICD) downregulates Wiskott-Aldrich syndrome protein (WASP)-family verprolin homologous protein 1 (WAVE1 or WASF1) as part of a negative feedback mechanism to limit Aβ production.
Signaling networks that regulate cell migration.
Horwitz et al., Charlottesville, United States. In Cold Spring Harb Perspect Biol, Aug 2015
Their effectors include actin regulators such as formins, members of the WASP/WAVE family and the Arp2/3 complex, and the myosin II motor protein.
Feedback regulation between plasma membrane tension and membrane-bending proteins organizes cell polarity during leading edge formation.
Itoh et al., Kōbe, Japan. In Nat Cell Biol, Jun 2015
Here, we demonstrate that FBP17, a membrane-bending protein and an activator of WASP/N-WASP-dependent actin nucleation, is a PM tension sensor involved in leading edge formation.
Human Immunodeficiencies Related to Defective APC/T Cell Interaction.
Benvenuti et al., Rozzano, Italy. In Front Immunol, 2014
The Wiskott-Aldrich syndrome (WAS) is a severe primary immunodeficiency caused by mutations in the Wiskott-Aldrich syndrome protein (WASp), a scaffold that promotes actin polymerization and links TCR stimulation to T cell activation.
A role for the small GTPase Rac1 in vaccinia actin-based motility.
Agaisse et al., Buenos Aires, Argentina. In Small Gtpases, 2014
Vaccinia virus dissemination relies on the recruitment of the nucleation promoting factor N-WASP underneath cell-associated extracellular virus (CEVs) and subsequent recruitment and activation of the ARP2/3 complex, a major actin nucleator of the host cell.
HIV-1 Infection of T Lymphocytes and Macrophages Affects Their Migration via Nef.
Maridonneau-Parini et al., Toulouse, France. In Front Immunol, 2014
Indeed, the mesenchymal migration involves podosomes, and Nef stabilizes these cell structures through the activation of the tyrosine kinase Hck, which in turn phosphorylates the Wiskott-Aldrich syndrome protein (WASP).
Capping protein regulators fine-tune actin assembly dynamics.
Cooper et al., Saint Louis, United States. In Nat Rev Mol Cell Biol, 2014
These proteins, including CARMIL (capping protein, ARP2/3 and myosin I linker), CD2AP (CD2-associated protein) and the WASH (WASP and SCAR homologue) complex subunit FAM21, recruit CP to specific subcellular locations and modulate its actin-capping activity via allosteric effects.
Steering cell migration: lamellipodium dynamics and the regulation of directional persistence.
Gautreau et al., Gif-sur-Yvette, France. In Nat Rev Mol Cell Biol, 2014
Recently, advances have been made in our understanding of positive and negative ARP2/3 regulators (such as the SCAR/WAVE (SCAR/WASP family verprolin-homologous protein) complex and Arpin, respectively) and of proteins that control actin branch stability (such as glial maturation factor (GMF)) or actin filament elongation (such as ENA/VASP proteins) in lamellipodium dynamics and cell migration.
Cardiac BIN1 folds T-tubule membrane, controlling ion flux and limiting arrhythmia.
Shaw et al., Los Angeles, United States. In Nat Med, 2014
We also found that T-tubule inner folds are rescued by expression of the BIN1 isoform BIN1+13+17, which promotes N-WASP-dependent actin polymerization to stabilize the T-tubule membrane at cardiac Z discs.
Wiskott-Aldrich syndrome protein controls antigen-presenting cell-driven CD4+ T-cell motility by regulating adhesion to intercellular adhesion molecule-1.
Dupré et al., Toulouse, France. In Immunology, 2012
WASP-deficient T cells migrated in a normal proportion towards CXCL12, CCL19 and CCL21, but displayed an increased adhesion and elongation on ICAM-1
Wiskott-Aldrich syndrome protein deficiency in innate immune cells leads to mucosal immune dysregulation and colitis in mice.
Snapper et al., Boston, United States. In Gastroenterology, 2012
WASP-deficient aberrant innate immune cells can render wild-type T cells severely colitogenic.
Wiskott-Aldrich syndrome protein (WASp) and N-WASp are involved in the regulation of NK-cell migration upon NKG2D activation.
López-Larrea et al., Oviedo, Spain. In Eur J Immunol, 2012
study describes that both N-WASp and WASp participate in the inhibition of NK-cell chemotaxis in response to NKG2D WASp engagement, and that this effect is not dependent on the regulation of F-actin dynamics
Ubiquitylation-dependent negative regulation of WASp is essential for actin cytoskeleton dynamics.
Barda-Saad et al., Ramat Gan, Israel. In Mol Cell Biol, 2012
data suggest that regulated degradation of activated WASp might be an efficient strategy by which the duration and localization of actin rearrangement and the intensity of T-cell activation are controlled.
Single-chain variable fragment intrabody impairs LPS-induced inflammatory responses by interfering with the interaction between the WASP N-terminal domain and Btk in macrophages.
Kitani et al., Tsukuba, Japan. In Biochem Biophys Res Commun, 2012
These observations strongly suggest that the phosphorylation of WASP by Btk plays a pivotal role in transducing the LPS signaling pathway in macrophages.
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