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High levels of oncomiR‐21 contribute to the senescence‐induced growth arrest in normal human cells and its knock‐down increases the replicative lifespan
Authors:Lucia Terlecki‐Zaniewicz  Carina Schreiner  Klaus Fortschegger  Martina W.‐F. Chang  Matthias Hackl  Rossella Monteforte  Harald Kühnel  Markus Schosserer  Florian Gruber  Erwin Tschachler  Marcel Scheideler  Regina Grillari‐Voglauer  Johannes Grillari  Matthias Wieser
Affiliation:1. Department of Biotechnology, BOKU‐VIBT University of Natural Resources and Life Sciences Vienna, , 1190 Vienna, Austria;2. CCRI ‐ Children's Cancer Research Institute, , 1090 Vienna, Austria;3. Institute of Physiology, Pathophysiology and Biophysics, Department of Biomedical Sciences, University of Veterinary Medicine Vienna, , A‐1210 Vienna, Austria;4. Department of Dermatology, Medical University of Vienna, , A‐1090 Vienna, Austria;5. C.E.R.I.E.S. ‐ Centre de Recherches et d'Investigations Epidermiques et Sensorielles, , 92200 Neuilly‐sur‐Seine, France;6. Institute for Genomics and Bioinformatics, Graz University of Technology, , 8010 Graz, Austria;7. Evercyte GmbH, , 1190 Vienna, Austria;8. Austrian Centre of Industrial Biotechnology (ACIB GmbH), , 1190 Vienna, Austria
Abstract:
Keywords:CDC25A  CDK2  cellular senescence  hyperoncogenic signal  microRNA  miR‐21     NFIB     p21
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