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dc.contributor.authorLucas, Julie Ann
dc.contributor.authorMiller, Andrew Todd
dc.contributor.authorAtherly, Luana O.
dc.contributor.authorBerg, Leslie J.
dc.date2022-08-11T08:09:01.000
dc.date.accessioned2022-08-23T16:15:37Z
dc.date.available2022-08-23T16:15:37Z
dc.date.issued2003-03-05
dc.date.submitted2008-11-05
dc.identifier.citation<p>Immunol Rev. 2003 Feb;191:119-38.</p>
dc.identifier.issn0105-2896 (Print)
dc.identifier.doi10.1034/j.1600-065X.2003.00029.x
dc.identifier.pmid12614356
dc.identifier.urihttp://hdl.handle.net/20.500.14038/34130
dc.description.abstractThree members of the Tec family kinases, Itk, Rlk and Tec, have been implicated in signaling downstream of the T cell receptor (TCR). The activity of these kinases in T cells has been shown to be important for the full activation of phospholipase C-gamma1 (PLC-gamma1). Disruption of Tec family signaling in Itk-/- and Rlk-/-Itk-/- mice has multiple effects on T cell development, cytokine production and T-helper cell differentiation. Furthermore, mice possessing mutations in signaling molecules upstream of PLC-gamma1, such as Src homology 2 (SH2) domain-containing phosphoprotein of 76 kDa (SLP-76), linker for activation of T cells (LAT) and Vav1, or in members of the nuclear factor for activated T cells (NFAT) family of transcription factors, which are downstream of PLC-gamma1, have been found to have similar phenotypes to Tec family-deficient mice, emphasizing the importance of this pathway in regulating T cell activation, differentiation and homeostasis.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12614356&dopt=Abstract">Link to article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1034/j.1600-065X.2003.00029.x
dc.titleThe role of Tec family kinases in T cell development and function
dc.typeJournal Article
dc.source.journaltitleImmunological reviews
dc.source.volume191
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/792
dc.identifier.contextkey661902
html.description.abstract<p>Three members of the Tec family kinases, Itk, Rlk and Tec, have been implicated in signaling downstream of the T cell receptor (TCR). The activity of these kinases in T cells has been shown to be important for the full activation of phospholipase C-gamma1 (PLC-gamma1). Disruption of Tec family signaling in Itk-/- and Rlk-/-Itk-/- mice has multiple effects on T cell development, cytokine production and T-helper cell differentiation. Furthermore, mice possessing mutations in signaling molecules upstream of PLC-gamma1, such as Src homology 2 (SH2) domain-containing phosphoprotein of 76 kDa (SLP-76), linker for activation of T cells (LAT) and Vav1, or in members of the nuclear factor for activated T cells (NFAT) family of transcription factors, which are downstream of PLC-gamma1, have been found to have similar phenotypes to Tec family-deficient mice, emphasizing the importance of this pathway in regulating T cell activation, differentiation and homeostasis.</p>
dc.identifier.submissionpathgsbs_sp/792
dc.contributor.departmentPathology
dc.contributor.departmentMorningside Graduate School of Biomedical Sciences
dc.source.pages119-38
dc.contributor.studentJulie Ann Lucas
dc.description.thesisprogramImmunology and Virology


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