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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2001-4-24
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pubmed:abstractText |
Cellular organization of the cytoskeleton, assembly of intracellular signaling complexes and movement of membrane receptors into supramolecular activation complexes (SMACs) are crucial prerequisites for lymphocyte activation and function. Full T-cell activation requires costimulatory signals in addition to antigen-mediated signals. Costimulatory signals facilitate T-cell activation by inducing SMAC formation, resulting in sustained signal transduction, cell-cycle progression and cytokine production. The guanine nucleotide exchange factor Vav1 and the Wiscott-Aldrich syndrome protein (WASP) regulate the actin cytoskeleton in T cells and also regulate SMAC formation. In mice lacking the E3 ubiquitin ligase Cbl-b, the Vav-WASP signaling pathway is active in the absence of costimulation resulting in deregulated cytoskeletal reorganization, enhanced priming and expansion of autoreactive T cells, and the development of autoimmunity. This review discusses the role of Cbl-b, Vav and WASP in the regulation of SMAC formation and the implications for the maintenance of tolerance and the development of autoimmunity.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adaptor Proteins, Signal Transducing,
http://linkedlifedata.com/resource/pubmed/chemical/CBLB protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Cell Cycle Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Macromolecular Substances,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-cbl,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-vav,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/Ubiquitin-Protein Ligases,
http://linkedlifedata.com/resource/pubmed/chemical/VAV1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/WAS protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Wiskott-Aldrich Syndrome Protein
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0962-8924
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
11
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
212-20
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:11316610-Adaptor Proteins, Signal Transducing,
pubmed-meshheading:11316610-Animals,
pubmed-meshheading:11316610-Autoimmunity,
pubmed-meshheading:11316610-Carrier Proteins,
pubmed-meshheading:11316610-Cell Cycle Proteins,
pubmed-meshheading:11316610-Cytoskeleton,
pubmed-meshheading:11316610-Humans,
pubmed-meshheading:11316610-Macromolecular Substances,
pubmed-meshheading:11316610-Models, Immunological,
pubmed-meshheading:11316610-Phosphoproteins,
pubmed-meshheading:11316610-Protein Structure, Tertiary,
pubmed-meshheading:11316610-Proteins,
pubmed-meshheading:11316610-Proto-Oncogene Proteins,
pubmed-meshheading:11316610-Proto-Oncogene Proteins c-cbl,
pubmed-meshheading:11316610-Proto-Oncogene Proteins c-vav,
pubmed-meshheading:11316610-Receptor Aggregation,
pubmed-meshheading:11316610-Receptors, Antigen, T-Cell,
pubmed-meshheading:11316610-Signal Transduction,
pubmed-meshheading:11316610-T-Lymphocytes,
pubmed-meshheading:11316610-Ubiquitin-Protein Ligases,
pubmed-meshheading:11316610-Wiskott-Aldrich Syndrome Protein
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pubmed:year |
2001
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pubmed:articleTitle |
Molecular controls of antigen receptor clustering and autoimmunity.
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pubmed:affiliation |
Dept of Medical Biophysics, Amgen Institute/Ontario Cancer Institute, University of Toronto, 620 University Avenue, M5G 2C1, Toronto, Ontario, Canada.
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pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
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