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http://purl.uniprot.org/citations/16636677http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16636677http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16636677http://www.w3.org/2000/01/rdf-schema#comment"Perpetual V(D)J recombinase activity involving multiple DNA double-strand break events in B-cell lineage leukemia and lymphoma cells may introduce secondary genetic aberrations leading towards malignant progression. Here, we investigated defective negative feedback signaling through the (pre-) B-cell receptor as a possible reason for deregulated V(D)J recombinase activity in B-cell malignancy. On studying 28 cases of pre-B-lymphoblastic leukemia and 27 B-cell lymphomas, expression of the (pre-) B-cell receptor-related linker molecule SLP65 (SH2 domain-containing lymphocyte protein of 65 kDa) was found to be defective in seven and five cases, respectively. SLP65 deficiency correlates with RAG1/2 expression and unremitting V(H) gene rearrangement activity. Reconstitution of SLP65 expression in SLP65-deficient leukemia and lymphoma cells results in downregulation of RAG1/2 expression and prevents both de novo V(H)-DJ(H) rearrangements and secondary V(H) replacement. We conclude that iterative V(H) gene rearrangement represents a frequent feature in B-lymphoid malignancy, which can be attributed to SLP65 deficiency in many cases."xsd:string
http://purl.uniprot.org/citations/16636677http://purl.org/dc/terms/identifier"doi:10.1038/sj.onc.1209520"xsd:string
http://purl.uniprot.org/citations/16636677http://purl.org/dc/terms/identifier"doi:10.1038/sj.onc.1209520"xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/author"Siebert R."xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/author"Siebert R."xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/author"Feldhahn N."xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/author"Feldhahn N."xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/author"Jumaa H."xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/author"Jumaa H."xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/author"Liedtke S."xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/author"Liedtke S."xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/author"Muschen M."xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/author"Muschen M."xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/author"Sprangers M."xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/author"Sprangers M."xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/name"Oncogene"xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/name"Oncogene"xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/pages"5180-5186"xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/pages"5180-5186"xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/title"SLP65 deficiency results in perpetual V(D)J recombinase activity in pre-B-lymphoblastic leukemia and B-cell lymphoma cells."xsd:string
http://purl.uniprot.org/citations/16636677http://purl.uniprot.org/core/title"SLP65 deficiency results in perpetual V(D)J recombinase activity in pre-B-lymphoblastic leukemia and B-cell lymphoma cells."xsd:string