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http://purl.uniprot.org/citations/15292262http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15292262http://www.w3.org/2000/01/rdf-schema#comment"Siglec-7 (p70/AIRM) and Siglec-9 are "CD33"-related siglecs expressed on natural killer (NK) cells and subsets of peripheral T cells. Like other inhibitory NK cell receptors, they contain immunoglobulin receptor family tyrosine-based inhibitory motifs in their cytoplasmic domains, and Siglec-7 has been demonstrated to negatively regulate NK cell activation. Based on reports of the presence of these siglecs on T cells, we sought to determine if they are capable of modulating T cell receptor (TCR) signaling using Jurkat T cells stably and transiently transfected with Siglec-7 or Siglec-9. Following either pervanadate stimulation or TCR engagement, both Siglecs exhibited increased tyrosine phosphorylation and recruitment of SHP-1. Effects of Siglec-7 and -9 were also evident in downstream events in the signaling pathway. Both siglecs reduced phosphorylation of Tyr319 on ZAP-70, known to play a pivotal role in up-regulation of gene transcription following TCR stimulation. There was also a corresponding decreased transcriptional activity of nuclear factor of activated T cells (NFAT) as determined using a luciferase reporter gene. Like all siglecs, Siglec-7 and -9 recognize sialic acid-containing glycans of glycoproteins and glycolipids as ligands. Mutation of the conserved Arg in the ligand binding site of Siglec-7 (Arg124) or Siglec-9 (Arg120) resulted in reduced inhibitory function in the NFAT/luciferase transcription assay, suggesting that ligand binding is required for optimal inhibition of TCR signaling. The combined results demonstrate that both Siglec-7 and Siglec-9 are capable of negative regulation of TCR signaling and that ligand binding is required for optimal activity."xsd:string
http://purl.uniprot.org/citations/15292262http://purl.org/dc/terms/identifier"doi:10.1074/jbc.m403538200"xsd:string
http://purl.uniprot.org/citations/15292262http://purl.uniprot.org/core/author"Ikehara Y."xsd:string
http://purl.uniprot.org/citations/15292262http://purl.uniprot.org/core/author"Paulson J.C."xsd:string
http://purl.uniprot.org/citations/15292262http://purl.uniprot.org/core/author"Ikehara S.K."xsd:string
http://purl.uniprot.org/citations/15292262http://purl.uniprot.org/core/date"2004"xsd:gYear
http://purl.uniprot.org/citations/15292262http://purl.uniprot.org/core/name"J Biol Chem"xsd:string
http://purl.uniprot.org/citations/15292262http://purl.uniprot.org/core/pages"43117-43125"xsd:string
http://purl.uniprot.org/citations/15292262http://purl.uniprot.org/core/title"Negative regulation of T cell receptor signaling by Siglec-7 (p70/AIRM) and Siglec-9."xsd:string
http://purl.uniprot.org/citations/15292262http://purl.uniprot.org/core/volume"279"xsd:string
http://purl.uniprot.org/citations/15292262http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/15292262
http://purl.uniprot.org/citations/15292262http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/15292262
http://purl.uniprot.org/uniprot/#_Q9Y336-mappedCitation-15292262http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15292262
http://purl.uniprot.org/uniprot/#_P43403-mappedCitation-15292262http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15292262
http://purl.uniprot.org/uniprot/#_Q9Y286-mappedCitation-15292262http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15292262
http://purl.uniprot.org/uniprot/Q9Y336http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/15292262
http://purl.uniprot.org/uniprot/P43403http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/15292262
http://purl.uniprot.org/uniprot/Q9Y286http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/15292262