DNA damage-induced cell death by apoptosis.

By W. Roos, B. Kaina. Trends in Molecular Medicine, 2006

1,534 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/1cc62554535ccb70e12217f291872ce427d328ae

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. Elias K. Michaelis
2. Simone Fulda
3. B. Kaina
4. W. Roos
5. Rajeshwar Prasad Sinha
6. A. Gorman
7. Afshin Samali

In Oncology

1. Elias K. Michaelis
2. Simone Fulda
3. B. Kaina
4. W. Roos
5. A. Gorman
6. Afshin Samali

Citations in the corpus

• Selective Neuronal Vulnerability to Oxidative Stress in the Brain (2010, positive): “…damage is insuffi cient, then damaged DNA accumulates, especially, in the promoter regions of protein-coding genes, and this can lead to transcriptional disruption of active genes, followed by cellular dysfunction and, ultimately, apoptosis (Hanawalt, 1994; Lu et al., 2004; Roos and Kaina, 2006).”
• DNA damage-induced cell death: from specific DNA lesions to the DNA damage response and apoptosis. (2013, background): “DNA damage most often activates the extrinsic death receptor apoptosis pathway (Fas, CD95, Apo-1) and/or the intrinsic mitochondrial apoptosis pathway [113].”
• Molecular Mechanisms of Ultraviolet Radiation-Induced DNA Damage and Repair (2010, background): “It was assumed that initial photoproducts are converted into DSBs during DNA replication, due to not a distinct process, that is, “collapse of replication forks” [93].”
• Tumor resistance to apoptosis (2009, background): “Following exposure to genotoxic substances, damage to DNA or to other critical molecules is considered to be a common initial event which is then transmitted by the cellular stress response to the activation of cellular effector systems such as the apoptotic machinery.(13) Various stress-inducible m”
• Cellular Stress Responses: Cell Survival and Cell Death (2010, background): “DSBs are produced directly or indirectly by many anticancer drugs, including DNA intercalating, alkylating or crosslinking agents, topoisomerase inhibitors, and nucleotide analogs [174].”