{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["6"],"submitter":["Poltz R"],"pubmed_abstract":["<h4>Background</h4>The genome is continuously attacked by a variety of agents that cause DNA damage. Recognition of DNA lesions activates the cellular DNA damage response (DDR), which comprises a network of signal transduction pathways to maintain genome integrity. In response to severe DNA damage, cells undergo apoptosis to avoid transformation into tumour cells, or alternatively, the cells enter permanent cell cycle arrest, called senescence. Most tumour cells have defects in pathways leading to DNA repair or apoptosis. In addition, apoptosis could be counteracted by nuclear factor kappa B (NF-κB), the main anti-apoptotic transcription factor in the DDR. Despite the high clinical relevance, the interplay of the DDR pathways is poorly understood. For therapeutic purposes DNA damage signal"],"journal":["BMC systems biology"],"pagination":["125"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3473366"],"repository":["biostudies-literature"],"pubmed_title":["Dynamics of p53 and NF-κB regulation in response to DNA damage and identification of target proteins suitable for therapeutic intervention."],"pmcid":["PMC3473366"],"pubmed_authors":["Poltz R","Naumann M"],"additional_accession":[]},"is_claimable":false,"name":"Dynamics of p53 and NF-κB regulation in response to DNA damage and identification of target proteins suitable for therapeutic intervention.","description":"<h4>Background</h4>The genome is continuously attacked by a variety of agents that cause DNA damage. Recognition of DNA lesions activates the cellular DNA damage response (DDR), which comprises a network of signal transduction pathways to maintain genome integrity. In response to severe DNA damage, cells undergo apoptosis to avoid transformation into tumour cells, or alternatively, the cells enter permanent cell cycle arrest, called senescence. Most tumour cells have defects in pathways leading to DNA repair or apoptosis. In addition, apoptosis could be counteracted by nuclear factor kappa B (NF-κB), the main anti-apoptotic transcription factor in the DDR. Despite the high clinical relevance, the interplay of the DDR pathways is poorly understood. For therapeutic purposes DNA damage signal","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 Sep","modification":"2025-04-18T11:53:40.969Z","creation":"2019-03-27T00:59:10Z"},"accession":"S-EPMC3473366","cross_references":{"pubmed":["22979979"],"doi":["10.1186/1752-0509-6-125"]}}