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{ <http://www.tkuhn.ch/bel2nanopub/RAqsJ697vpTLGHY-6RrwVRSYhCtPTmGgzL2IJhrsEqYZg#_2> ?p ?o ?g. }
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Most strikingly, upon cell cycle arrest resulting from genotoxic stress and p53 activation, TFII-I is ubiquitinated and targeted for proteasomal degradation in a p53- and ATM (ataxia telangiectasia mutated)-dependent manner.
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