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http://purl.uniprot.org/citations/29581031http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29581031http://www.w3.org/2000/01/rdf-schema#comment"IL-7 is required for T cell differentiation and mature T cell homeostasis and promotes pro-B cell proliferation and survival. Tyrosine phosphorylation plays a central role in IL-7 signaling. We identified by two-dimensional electrophoresis followed by anti-phosphotyrosine immunoblotting and mass spectrometry sixteen tyrosine phosphorylated proteins from the IL-7-dependent cell line D1. IL-7 stimulation induced the phosphorylation of the proteins STI1, ATIC and hnRNPH, involved in pathways related to survival, proliferation and gene expression, respectively, and increased the phosphorylation of CrkL, a member of a family of adaptors including the highly homologous Crk isoforms CrkII and CrkI, important in multiple signaling pathways. We observed an increased phosphorylation of CrkL in murine pro-B cells and in murine and human T cells. In addition, IL-7 increased the association of CrkL with the transcription factor Stat5, essential for IL-7 pro-survival activity. The selective tyrosine kinase inhibitor Imatinib. counteracted the IL-7 pro-survival effect in D1 cells and decreased CrkL phosphorylation. These data suggested that CrkL could play a pro-survival role in IL-7-mediated signaling. We observed that pro-B cells also expressed, in addition to CrkL, the Crk isoforms CrkII and CrkI and therefore utilized pro-B cells conditionally deficient in all three to evaluate the role of these proteins. The observation that the IL-7 pro-survival effect was reduced in Crk/CrkL conditionally-deficient pro-B cells further pointed to a pro-survival role of these adaptors. To further evaluate the role of these proteins, gene expression studies were performed in Crk/CrkL conditionally-deficient pro-B cells. IL-7 decreased the transcription of the receptor LAIR1, which inhibits B cell proliferation, in a Crk/CrkL-dependent manner, suggesting that the Crk family of proteins may promote pro-B cell proliferation. Our data contribute to the understanding of IL-7 signaling and suggest the involvement of Crk family proteins in pathways promoting survival and proliferation."xsd:string
http://purl.uniprot.org/citations/29581031http://purl.org/dc/terms/identifier"doi:10.1016/j.cellsig.2018.03.008"xsd:string
http://purl.uniprot.org/citations/29581031http://purl.uniprot.org/core/author"Bonetto V."xsd:string
http://purl.uniprot.org/citations/29581031http://purl.uniprot.org/core/author"Li W."xsd:string
http://purl.uniprot.org/citations/29581031http://purl.uniprot.org/core/author"Jiang Q."xsd:string
http://purl.uniprot.org/citations/29581031http://purl.uniprot.org/core/author"Guszczynski T."xsd:string
http://purl.uniprot.org/citations/29581031http://purl.uniprot.org/core/author"Durum S.K."xsd:string
http://purl.uniprot.org/citations/29581031http://purl.uniprot.org/core/author"Massignan T."xsd:string
http://purl.uniprot.org/citations/29581031http://purl.uniprot.org/core/author"Hixon J.A."xsd:string
http://purl.uniprot.org/citations/29581031http://purl.uniprot.org/core/author"Merchant A."xsd:string
http://purl.uniprot.org/citations/29581031http://purl.uniprot.org/core/author"Hodge D.L."xsd:string
http://purl.uniprot.org/citations/29581031http://purl.uniprot.org/core/author"Aiello F.B."xsd:string
http://purl.uniprot.org/citations/29581031http://purl.uniprot.org/core/author"Procopio A.D."xsd:string
http://purl.uniprot.org/citations/29581031http://purl.uniprot.org/core/author"Di Lisio C."xsd:string
http://purl.uniprot.org/citations/29581031http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/29581031http://purl.uniprot.org/core/name"Cell Signal"xsd:string
http://purl.uniprot.org/citations/29581031http://purl.uniprot.org/core/pages"131-141"xsd:string
http://purl.uniprot.org/citations/29581031http://purl.uniprot.org/core/title"IL-7-induced phosphorylation of the adaptor Crk-like and other targets."xsd:string
http://purl.uniprot.org/citations/29581031http://purl.uniprot.org/core/volume"47"xsd:string
http://purl.uniprot.org/citations/29581031http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/29581031
http://purl.uniprot.org/citations/29581031http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/29581031
http://purl.uniprot.org/uniprot/P56480#attribution-6666ABCD01A62641B1F644E2416B7138http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/29581031
http://purl.uniprot.org/uniprot/P63038#attribution-6666ABCD01A62641B1F644E2416B7138http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/29581031
http://purl.uniprot.org/uniprot/P47941#attribution-19BAACFCCA4CA2E84404B14679B3385Chttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/29581031