title: MKK7 and ARF: new players in the DNA damage response scenery.
abstract: Sensing, integrating, and processing of stressogenic signals must be followed by accurate differential response(s) for a cell to survive and avoid malignant transformation. The DNA damage response (DDR) pathway is vital in this process, as it deals with genotoxic/oncogenic insults, having p53 as a nodal effector that performs most of the above tasks. Accumulating data reveal that other pathways are also involved in the same or similar processes, conveying also to p53. Emerging questions are if, how, and when these additional pathways communicate with the DDR axis. Two such stress response pathways, involving the MKK7 stress-activated protein kinase (SAPK) and ARF, have been shown to be interlocked with the ATM/ATR-regulated DDR axis in a highly ordered manner. This creates a new landscape in the DDR orchestrated response to genotoxic/oncogenic insults that is currently discussed.
authors.affiliation: Molecular Carcinogenesis Group; Department of Histology and Embryology; School of Medicine; University of Athens; Athens, Greece.
authors.forename: Athanassios
authors.initials: A
authors.lastname: Kotsinas
authors.affiliation: Molecular Carcinogenesis Group; Department of Histology and Embryology; School of Medicine; University of Athens; Athens, Greece.
authors.forename: Panagiota
authors.initials: P
authors.lastname: Papanagnou
authors.affiliation: Molecular Carcinogenesis Group; Department of Histology and Embryology; School of Medicine; University of Athens; Athens, Greece.
authors.forename: Panagiotis
authors.initials: P
authors.lastname: Galanos
authors.affiliation: Howard Hughes Medical Institute; Laboratory of Mammalian Cell Biology and Development; The Rockefeller University; New York, NY USA.
authors.forename: Daniel
authors.initials: D
authors.lastname: Schramek
authors.affiliation: Faculty Institute of Cancer Sciences; University of Manchester; Manchester Academic Health Science Centre; Manchester, UK; Manchester Centre for Cellular Metabolism; University of Manchester; Manchester Academic Health Science Centre; Manchester, UK.
authors.forename: Paul
authors.initials: P
authors.lastname: Townsend
authors.affiliation: IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences; Vienna, Austria.
authors.forename: Josef M
authors.initials: JM
authors.lastname: Penninger
authors.affiliation: Danish Cancer Society Research Center; Copenhagen, Denmark; Institute of Molecular and Translational Medicine; Faculty of Medicine and Dentistry; Palacky University; Olomouc, Czech Republic.
authors.forename: Jiri
authors.initials: J
authors.lastname: Bartek
authors.affiliation: Molecular Carcinogenesis Group; Department of Histology and Embryology; School of Medicine; University of Athens; Athens, Greece; Faculty Institute of Cancer Sciences; University of Manchester; Manchester Academic Health Science Centre; Manchester, UK; Manchester Centre for Cellular Metabolism; University of Manchester; Manchester Academic Health Science Centre; Manchester, UK; Biomedical Research Foundation; Academy of Athens; Athens, Greece.
authors.forename: Vassilis G
authors.initials: VG
authors.lastname: Gorgoulis
mesh_terms: D000818:Animals; D064007:Ataxia Telangiectasia Mutated Proteins / Q000378:metabolism; D004249:DNA Damage; D004260:DNA Repair; D006801:Humans; D048688:MAP Kinase Kinase 7 / Q000378:metabolism*; D009857:Oncogenes; D010766:Phosphorylation; D016364:Reading Frames; D015398:Signal Transduction; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D016159:Tumor Suppressor Protein p53; C576324:ATM protein, human; C576597:ATR protein, human; D064007:Ataxia Telangiectasia Mutated Proteins; D048051:p38 Mitogen-Activated Protein Kinases; D048688:MAP Kinase Kinase 7; C482569:MAP2K7 protein, human
keywords: ARF; DNA damage response; MKK7; Wip-1; anti-tumor barrier; feedback loop; p38 MAPK; p53; replication stress; senescence