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http://purl.uniprot.org/citations/21209924http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21209924http://www.w3.org/2000/01/rdf-schema#comment"To generate high affinity antibodies during an immune response, B cells undergo somatic hypermutation (SHM) of their immunoglobulin genes. Error-prone translesion synthesis (TLS) DNA polymerases have been reported to be responsible for all mutations at template A/T and at least a fraction of G/C transversions. In contrast to A/T mutations which depend on PCNA ubiquitination, it remains unclear how G/C transversions are regulated during SHM. Several lines of evidence indicate a mechanistic link between the Fanconi Anemia (FA) pathway and TLS. To investigate the contribution of the FA pathway in SHM we analyzed FancG-deficient B cells. B cells deficient for FancG, an essential member of the FA core complex, were hypersensitive to treatment with cross-linking agents. However, the frequencies and nucleotide exchange spectra of SHM remained comparable between wild-type and FancG-deficient B cells. These data indicate that the FA pathway is not involved in regulating the outcome of SHM in mammals. In addition, the FA pathway appears dispensable for class switch recombination."xsd:string
http://purl.uniprot.org/citations/21209924http://purl.org/dc/terms/identifier"doi:10.1371/journal.pone.0015236"xsd:string
http://purl.uniprot.org/citations/21209924http://purl.uniprot.org/core/author"Jacobs H."xsd:string
http://purl.uniprot.org/citations/21209924http://purl.uniprot.org/core/author"van den Berk P.C."xsd:string
http://purl.uniprot.org/citations/21209924http://purl.uniprot.org/core/author"Krijger P.H."xsd:string
http://purl.uniprot.org/citations/21209924http://purl.uniprot.org/core/author"Wit N."xsd:string
http://purl.uniprot.org/citations/21209924http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/21209924http://purl.uniprot.org/core/name"PLoS One"xsd:string
http://purl.uniprot.org/citations/21209924http://purl.uniprot.org/core/pages"e15236"xsd:string
http://purl.uniprot.org/citations/21209924http://purl.uniprot.org/core/title"The Fanconi anemia core complex is dispensable during somatic hypermutation and class switch recombination."xsd:string
http://purl.uniprot.org/citations/21209924http://purl.uniprot.org/core/volume"5"xsd:string
http://purl.uniprot.org/citations/21209924http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/21209924
http://purl.uniprot.org/citations/21209924http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/21209924
http://purl.uniprot.org/uniprot/#_A4QPC9-mappedCitation-21209924http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21209924
http://purl.uniprot.org/uniprot/#_B9EJ17-mappedCitation-21209924http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21209924
http://purl.uniprot.org/uniprot/#_Q80X51-mappedCitation-21209924http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21209924
http://purl.uniprot.org/uniprot/#_Q8VHS1-mappedCitation-21209924http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21209924
http://purl.uniprot.org/uniprot/#_Q9EQR6-mappedCitation-21209924http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21209924
http://purl.uniprot.org/uniprot/B9EJ17http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/21209924
http://purl.uniprot.org/uniprot/Q9EQR6http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/21209924
http://purl.uniprot.org/uniprot/A4QPC9http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/21209924
http://purl.uniprot.org/uniprot/Q80X51http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/21209924
http://purl.uniprot.org/uniprot/Q8VHS1http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/21209924