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dc.contributor.authorBerg, Leslie J.
dc.contributor.authorFinkelstein, Lisa D.
dc.contributor.authorLucas, Julie Ann
dc.contributor.authorSchwartzberg, Pamela L.
dc.date2022-08-11T08:09:02.000
dc.date.accessioned2022-08-23T16:16:21Z
dc.date.available2022-08-23T16:16:21Z
dc.date.issued2005-03-18
dc.date.submitted2008-07-16
dc.identifier.citationAnnu Rev Immunol. 2005;23:549-600. <a href="http://dx.doi.org/10.1146/annurev.immunol.22.012703.104743">Link to article on publisher's site</a>
dc.identifier.issn0732-0582 (Print)
dc.identifier.doi10.1146/annurev.immunol.22.012703.104743
dc.identifier.pmid15771581
dc.identifier.urihttp://hdl.handle.net/20.500.14038/34309
dc.description.abstractThe Tec family tyrosine kinases are now recognized as important mediators of antigen receptor signaling in lymphocytes. Three members of this family, Itk, Rlk, and Tec, are expressed in T cells and activated in response to T cell receptor (TCR) engagement. Although initial studies demonstrated a role for these proteins in TCR-mediated activation of phospholipase C-gamma, recent data indicate that Tec family kinases also regulate actin cytoskeletal reorganization and cellular adhesion following TCR stimulation. In addition, Tec family kinases are activated downstream of G protein-coupled chemokine receptors, where they play parallel roles in the regulation of Rho GTPases, cell polarization, adhesion, and migration. In all these systems, however, Tec family kinases are not essential signaling components, but instead function to modulate or amplify signaling pathways. Although they quantitatively reduce proximal signaling, mutations that eliminate Tec family kinases in T cells nonetheless qualitatively alter T cell development and differentiation.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15771581&dopt=Abstract ">Link to article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1146/annurev.immunol.22.012703.104743
dc.subjectAnimals; Antigens, CD28; Enzyme Activation; Humans; Mice; Models, Immunological; Molecular Structure; Protein Structure, Tertiary; Protein-Tyrosine Kinases; Receptors, Antigen, T-Cell; Signal Transduction; T-Lymphocytes
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleTec family kinases in T lymphocyte development and function
dc.typeJournal Article
dc.source.journaltitleAnnual review of immunology
dc.source.volume23
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/96
dc.identifier.contextkey549658
html.description.abstract<p>The Tec family tyrosine kinases are now recognized as important mediators of antigen receptor signaling in lymphocytes. Three members of this family, Itk, Rlk, and Tec, are expressed in T cells and activated in response to T cell receptor (TCR) engagement. Although initial studies demonstrated a role for these proteins in TCR-mediated activation of phospholipase C-gamma, recent data indicate that Tec family kinases also regulate actin cytoskeletal reorganization and cellular adhesion following TCR stimulation. In addition, Tec family kinases are activated downstream of G protein-coupled chemokine receptors, where they play parallel roles in the regulation of Rho GTPases, cell polarization, adhesion, and migration. In all these systems, however, Tec family kinases are not essential signaling components, but instead function to modulate or amplify signaling pathways. Although they quantitatively reduce proximal signaling, mutations that eliminate Tec family kinases in T cells nonetheless qualitatively alter T cell development and differentiation.</p>
dc.identifier.submissionpathgsbs_sp/96
dc.contributor.departmentDepartment of Pathology
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages549-600


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