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http://purl.uniprot.org/citations/19927127http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19927127http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19927127http://www.w3.org/2000/01/rdf-schema#comment"Senescence is an irreversible cell-cycle arrest that is elicited by a wide range of factors, including replicative exhaustion. Emerging evidences suggest that cellular senescence contributes to ageing and acts as a tumour suppressor mechanism. To identify novel genes regulating senescence, we performed a loss-of-function screen on normal human diploid fibroblasts. We show that downregulation of the AMPK-related protein kinase 5 (ARK5 or NUAK1) results in extension of the cellular replicative lifespan. Interestingly, the levels of NUAK1 are upregulated during senescence whereas its ectopic expression triggers a premature senescence. Cells that constitutively express NUAK1 suffer gross aneuploidies and show diminished expression of the genomic stability regulator LATS1, whereas depletion of NUAK1 with shRNA exerts opposite effects. Interestingly, a dominant-negative form of LATS1 phenocopies NUAK1 effects. Moreover, we show that NUAK1 phosphorylates LATS1 at S464 and this has a role in controlling its stability. In summary, our work highlights a novel role for NUAK1 in the control of cellular senescence and cellular ploidy."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.org/dc/terms/identifier"doi:10.1038/emboj.2009.342"xsd:string
http://purl.uniprot.org/citations/19927127http://purl.org/dc/terms/identifier"doi:10.1038/emboj.2009.342"xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Martinez D."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Martinez D."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"de Launoit Y."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"de Launoit Y."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Navaratnam N."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Navaratnam N."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Carling D."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Carling D."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Da Costa M."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Da Costa M."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Bernard D."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Bernard D."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Gil J."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Gil J."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Augert A."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Augert A."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Abbadie C."xsd:string
http://purl.uniprot.org/citations/19927127http://purl.uniprot.org/core/author"Abbadie C."xsd:string