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The robust cellular response to DNA damage (DNA damage response or DDR) comprises multiple intertwined signaling networks that function in concert to optimize the manner in which a cell reacts to genotoxic stress. Downstream DDR signaling depends on two main upstream activators—the PI3K-related protein kinases ATM and ATR, whose respective activation by distinct types of DNA damage (DD) leads to a rapid phosphorylation of multiple proteins involved in processes such as DNA repair, cell-cycle arrest and programmed cell death (reviewed in Jackson and Bartek1, Lavin2, Cimprich and Cortez3).
MRE11 Homologue Protein, Antibiotics, Antineoplastic, DNA Repair, Tumor Suppressor Proteins, Apoptosis, Cell Cycle Proteins, Ataxia Telangiectasia Mutated Proteins, Protein Serine-Threonine Kinases, DNA-Binding Proteins, Doxorubicin, Humans, Proto-Oncogene Proteins c-abl, DNA Damage, Signal Transduction
MRE11 Homologue Protein, Antibiotics, Antineoplastic, DNA Repair, Tumor Suppressor Proteins, Apoptosis, Cell Cycle Proteins, Ataxia Telangiectasia Mutated Proteins, Protein Serine-Threonine Kinases, DNA-Binding Proteins, Doxorubicin, Humans, Proto-Oncogene Proteins c-abl, DNA Damage, Signal Transduction
citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 40 | |
popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Top 10% | |
influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 10% | |
impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 10% |