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http://purl.uniprot.org/citations/9454332http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/9454332http://www.w3.org/2000/01/rdf-schema#comment"Normal human cells undergo a finite number of cell divisions and ultimately enter a nondividing state called replicative senescence. It has been proposed that telomere shortening is the molecular clock that triggers senescence. To test this hypothesis, two telomerase-negative normal human cell types, retinal pigment epithelial cells and foreskin fibroblasts, were transfected with vectors encoding the human telomerase catalytic subunit. In contrast to telomerase-negative control clones, which exhibited telomere shortening and senescence, telomerase-expressing clones had elongated telomeres, divided vigorously, and showed reduced straining for beta-galactosidase, a biomarker for senescence. Notably, the telomerase-expressing clones have a normal karyotype and have already exceeded their normal life-span by at least 20 doublings, thus establishing a causal relationship between telomere shortening and in vitro cellular senescence. The ability to maintain normal human cells in a phenotypically youthful state could have important applications in research and medicine."xsd:string
http://purl.uniprot.org/citations/9454332http://purl.org/dc/terms/identifier"doi:10.1126/science.279.5349.349"xsd:string
http://purl.uniprot.org/citations/9454332http://purl.uniprot.org/core/author"Ouellette M."xsd:string
http://purl.uniprot.org/citations/9454332http://purl.uniprot.org/core/author"Chiu C.P."xsd:string
http://purl.uniprot.org/citations/9454332http://purl.uniprot.org/core/author"Morin G.B."xsd:string
http://purl.uniprot.org/citations/9454332http://purl.uniprot.org/core/author"Shay J.W."xsd:string
http://purl.uniprot.org/citations/9454332http://purl.uniprot.org/core/author"Wright W.E."xsd:string
http://purl.uniprot.org/citations/9454332http://purl.uniprot.org/core/author"Lichtsteiner S."xsd:string
http://purl.uniprot.org/citations/9454332http://purl.uniprot.org/core/author"Harley C.B."xsd:string
http://purl.uniprot.org/citations/9454332http://purl.uniprot.org/core/author"Holt S.E."xsd:string
http://purl.uniprot.org/citations/9454332http://purl.uniprot.org/core/author"Bodnar A.G."xsd:string
http://purl.uniprot.org/citations/9454332http://purl.uniprot.org/core/author"Frolkis M."xsd:string
http://purl.uniprot.org/citations/9454332http://purl.uniprot.org/core/date"1998"xsd:gYear
http://purl.uniprot.org/citations/9454332http://purl.uniprot.org/core/name"Science"xsd:string
http://purl.uniprot.org/citations/9454332http://purl.uniprot.org/core/pages"349-352"xsd:string
http://purl.uniprot.org/citations/9454332http://purl.uniprot.org/core/title"Extension of life-span by introduction of telomerase into normal human cells."xsd:string
http://purl.uniprot.org/citations/9454332http://purl.uniprot.org/core/volume"279"xsd:string
http://purl.uniprot.org/citations/9454332http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/9454332
http://purl.uniprot.org/citations/9454332http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/9454332
http://purl.uniprot.org/uniprot/O14746#attribution-DC20EBB7B54B0FF89A03CC623C5A59B4http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/9454332