نتایج جستجو برای: ژن wasp

تعداد نتایج: 21477  

2010
Lisa S. Westerberg Parool Meelu Marisa Baptista Michelle A. Eston David A. Adamovich Vinicius Cotta-de-Almeida Brian Seed Michael K. Rosen Peter Vandenberghe Adrian J. Thrasher Christoph Klein Frederick W. Alt Scott B. Snapper

X-linked neutropenia (XLN) is caused by activating mutations in the Wiskott-Aldrich syndrome protein (WASP) that result in aberrant autoinhibition. Although patients with XLN appear to have only defects in myeloid lineages, we hypothesized that activating mutations of WASP are likely to affect the immune system more broadly. We generated mouse models to assess the role of activating WASP mutati...

Journal: :Blood 2001
A Shcherbina H Miki D M Kenney F S Rosen T Takenawa E Remold-O'Donnell

Mutations of Wiskott-Aldrich syndrome protein (WASP) underlie the severe thrombocytopenia and immunodeficiency of the Wiskott-Aldrich syndrome. WASP, a specific blood cell protein, and its close homologue, the broadly distributed N-WASP, function in dynamic actin polymerization processes. Here it is demonstrated that N-WASP is expressed along with WASP, albeit at low levels, in human blood cell...

Journal: :Blood 2002
Maxim I Lutskiy Yoji Sasahara Dianne M Kenney Fred S Rosen Eileen Remold-O'Donnell

Wiskott-Aldrich syndrome (WAS) is an X-linked disease characterized by thrombocytopenia, eczema, and various degrees of immune deficiency. Carriers of mutated WASP have nonrandom X chromosome inactivation in their blood cells and are disease-free. We report data on a 14-month-old girl with a history of WAS in her family who presented with thrombocytopenia, small platelets, and immunologic dysfu...

2016
Marisa A P Baptista Marton Keszei Mariana Oliveira Karen K S Sunahara John Andersson Carin I M Dahlberg Austen J Worth Agne Liedén I-Chun Kuo Robert P A Wallin Scott B Snapper Liv Eidsmo Annika Scheynius Mikael C I Karlsson Gerben Bouma Siobhan O Burns Mattias N E Forsell Adrian J Thrasher Susanne Nylén Lisa S Westerberg

Wiskott-Aldrich syndrome (WAS) is caused by loss-of-function mutations in the WASp gene. Decreased cellular responses in WASp-deficient cells have been interpreted to mean that WASp directly regulates these responses in WASp-sufficient cells. Here, we identify an exception to this concept and show that WASp-deficient dendritic cells have increased activation of Rac2 that support cross-presentat...

2007
Peter Van Der Stok

This document describes the State of the Art in Wireless sensor networks as perceived by the WASP consortium. After a description of the advance in the domains of the work-packages, a section continues with describing the State of the Art within the consortium for the given work-package. The document concludes with the extensions to the State of the Art the consortium will peruse in the coming ...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2016
Max Rodnick-Smith Qing Luan Su-Ling Liu Brad J Nolen

The Arp2/3 (Actin-related proteins 2/3) complex is activated by WASP (Wiskott-Aldrich syndrome protein) family proteins to nucleate branched actin filaments that are important for cellular motility. WASP recruits actin monomers to the complex and stimulates movement of Arp2 and Arp3 into a "short-pitch" conformation that mimics the arrangement of actin subunits within filaments. The relative co...

Journal: :Journal of immunology 2003
Rong Zeng Judy L Cannon Robert T Abraham Michael Way Daniel D Billadeau Julie Bubeck-Wardenberg Janis K Burkhardt

We have shown previously that Wiskott-Aldrich syndrome protein (WASP) activation at the site of T cell-APC interaction is a two-step process, with recruitment dependent on the proline-rich domain and activation dependent on binding of Cdc42-GTP to the GTPase binding domain. Here, we show that WASP recruitment occurs through binding to the C-terminal Src homology 3 domain of Nck. In contrast, WA...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2005
Luisa M Stamm Melissa A Pak J Hiroshi Morisaki Scott B Snapper Klemens Rottner Silvia Lommel Eric J Brown

Mycobacterium marinum, a natural pathogen of fish and frogs and an occasional pathogen of humans, is capable of inducing actin tail formation within the cytoplasm of macrophages, leading to actin-based motility and intercellular spread. Actin tail formation by M. marinum is markedly reduced in macrophages deficient in the Wiskott-Aldrich syndrome protein (WASP), which still contain the closely ...

Journal: :Blood 2001
A Oda H D Ochs L A Lasky S Spencer K Ozaki M Fujihara M Handa K Ikebuchi H Ikeda

Wiskott-Aldrich syndrome (WAS) and X-linked thrombocytopenia are caused by mutations of the WAS protein (WASP) gene. WASP may be involved in the regulation of podosome, an actin-rich dynamic cell adhesion structure formed by various types of cells. The molecular links between WASP and podosomes or other cell adhesion structures are unknown. Platelets express an SH2-SH3 adapter molecule, CrkL, t...

Journal: :The Journal of biological chemistry 2014
Haein Park Athanassios Dovas Samer Hanna Claire Lastrucci Celine Cougoule Romain Guiet Isabelle Maridonneau-Parini Dianne Cox

We have shown previously that tyrosine phosphorylation of Wiskott-Aldrich syndrome protein (WASP) is important for diverse macrophage functions including phagocytosis, chemotaxis, podosome dynamics, and matrix degradation. However, the specific tyrosine kinase mediating WASP phosphorylation is still unclear. Here, we provide evidence that Hck, which is predominantly expressed in leukocytes, can...

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