PubMed:10074432
Annnotations
jnlpba-st-training
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genia-medco-coref
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pubmed-sentences-benchmark
{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":114},"obj":"Sentence"},{"id":"S2","span":{"begin":115,"end":262},"obj":"Sentence"},{"id":"S3","span":{"begin":263,"end":404},"obj":"Sentence"},{"id":"S4","span":{"begin":405,"end":591},"obj":"Sentence"},{"id":"S5","span":{"begin":592,"end":703},"obj":"Sentence"},{"id":"S6","span":{"begin":704,"end":810},"obj":"Sentence"},{"id":"S7","span":{"begin":811,"end":849},"obj":"Sentence"},{"id":"S8","span":{"begin":850,"end":1011},"obj":"Sentence"},{"id":"S9","span":{"begin":1012,"end":1170},"obj":"Sentence"},{"id":"S10","span":{"begin":1171,"end":1387},"obj":"Sentence"}],"text":"A direct interaction between the adaptor protein Cbl-b and the kinase zap-70 induces a positive signal in T cells.\nEngagement of the T-cell receptor (TCR)-CD3 complex induces a rapid increase in the activities of Src-family and Syk/Zap-70-family kinases [1] [2]. These activated kinases then induce the tyrosine phosphorylation of multiple intracellular proteins, eventually leading to T-cell activation. One of the prominent substrates for these kinases is the adaptor protein Cbl [3] and recent studies suggest that Cbl negatively regulates upstream kinases such as Syk and Zap-70 [4] [5]. Cbl-b, a homologue of Cbl, is widely expressed in many tissues and cells including hematopoietic cells [6] [7]. Cbl-b undergoes rapid tyrosine phosphorylation upon stimulation of the TCR and cytokine receptors [8] [9]. The role of Cbl-b is unclear, however. Here, we show that overexpression of Cbl-b in T cells induced the constitutive activation of the transcription factor nuclear factor of activated T cells (NFAT). A loss-of-function mutation in Cbl-b disrupted the interaction between Cbl-b and Zap-70 and nearly completely abrogated the Cbl-b-mediated activation of NFAT. Unlike the proposed role of Cbl as a negative regulator, our results suggest that the Cbl homologue Cbl-b has a positive role in T-cell signaling, most likely via a direct interaction with the upstream kinase Zap-70."}
GENIAcorpus
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