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All rights reserved." } ], "http://purl.org/dc/elements/1.1/title" : [ { "@value" : "BEL Framework Large Corpus Document" } ], "http://purl.org/pav/authoredBy" : [ { "@id" : "http://www.tkuhn.ch/bel2nanopub/RAkAR3zQmShu5ppetKhwdj_Qf36_t_q755c46dJuFKd3A#_3" } ], "http://purl.org/pav/version" : [ { "@value" : "1.4" } ] }, { "@id" : "http://www.tkuhn.ch/bel2nanopub/RAkAR3zQmShu5ppetKhwdj_Qf36_t_q755c46dJuFKd3A#_2", "http://www.w3.org/ns/prov#value" : [ { "@value" : "Ultraviolet radiation is a potent inducer of apoptosis, whereas autocrine nerve growth factor protects human keratinocytes from programmed cell death. To evaluate the role of nerve growth factor in the mechanisms of ultraviolet B-induced apoptosis, cultured human keratinocytes were ultraviolet B irradiated following pretreatment with K252, a specific inhibitor of the tyrosine kinase high-affinity nerve growth factor receptor. Here we report that the addition of K252 significantly enhanced keratinocyte apoptosis. We then transfected normal human keratinocytes with pNUT-hNGF. Nerve growth factor overexpressing keratinocytes secreted the highest amounts of nerve growth factor in culture supernatants, were more viable, and had a higher rate of proliferation than mock-transfected cells. Whereas ultraviolet B radiation downregulated nerve growth factor mRNA and protein as well as the tyrosine kinase high-affinity nerve growth factor receptor in normal keratinocytes, it failed to do so in nerve growth factor-transfected cells. Moreover, nerve growth factor overexpressing keratinocytes were partially resistant to apoptosis induced by increasing doses of ultraviolet B at 24 and 48 h. These results indicate that downregulation of nerve growth factor function plays an important part in the mechanisms of ultraviolet B-induced apoptosis in human keratinocytes. In addition, ultraviolet B caused a decrease in BCL-2 and BCL-xL expression in mock-transfected keratinocytes, but not in nerve growth factor overexpressing cells. Finally, nerve growth factor prevented the cleavage of the enzyme poly(ADP-ribose) polymerase induced in human keratinocytes by ultraviolet B. These results are consistent with a model whereby the autocrine nerve growth factor protects human keratinocytes from ultraviolet B-induced apoptosis by maintaining constant levels of BCL-2 and BCL-xL, which in turn might block caspase activation." } ], "http://www.w3.org/ns/prov#wasQuotedFrom" : [ { "@id" : "http://www.ncbi.nlm.nih.gov/pubmed/10594731" } ] }, { "@id" : "http://www.tkuhn.ch/bel2nanopub/RAkAR3zQmShu5ppetKhwdj_Qf36_t_q755c46dJuFKd3A#_3", "http://www.w3.org/2000/01/rdf-schema#label" : [ { "@value" : "Selventa" } ] }, { "@id" : "http://www.tkuhn.ch/bel2nanopub/RAkAR3zQmShu5ppetKhwdj_Qf36_t_q755c46dJuFKd3A#assertion", "http://www.w3.org/ns/prov#hadPrimarySource" : [ { "@id" : "http://www.ncbi.nlm.nih.gov/pubmed/10594731" } ], "http://www.w3.org/ns/prov#wasDerivedFrom" : [ { "@id" : "http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel" }, { "@id" : "http://www.tkuhn.ch/bel2nanopub/RAkAR3zQmShu5ppetKhwdj_Qf36_t_q755c46dJuFKd3A#_2" } ] } ], "@id" : "http://www.tkuhn.ch/bel2nanopub/RAkAR3zQmShu5ppetKhwdj_Qf36_t_q755c46dJuFKd3A#provenance" }, { "@graph" : [ { "@id" : "http://www.tkuhn.ch/bel2nanopub/RAkAR3zQmShu5ppetKhwdj_Qf36_t_q755c46dJuFKd3A", "http://purl.org/dc/terms/created" : [ { "@type" : "http://www.w3.org/2001/XMLSchema#dateTime", "@value" : "2014-07-03T14:29:49.473+02:00" } ], "http://purl.org/pav/createdBy" : [ { "@id" : "http://orcid.org/0000-0001-6818-334X" }, { "@id" : "http://orcid.org/0000-0002-1267-0234" } ] } ], "@id" : "http://www.tkuhn.ch/bel2nanopub/RAkAR3zQmShu5ppetKhwdj_Qf36_t_q755c46dJuFKd3A#pubinfo" } ]