Results 231 to 240 of about 57,844 (267)
Impeding the NHEJ Pathway for Overcoming Radioresistance in the Context of Precision Radiotherapy of Cancer. [PDF]
Niculae DA +3 more
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Synthetic lethality and DNA damage response targeting in cancer stem cells: a comprehensive review. [PDF]
Sayed U +8 more
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Genome-wide screen reveals dependence of break induced replication on several distinct checkpoints. [PDF]
Liu L +8 more
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Total Synthesis of the G2/M DNA Damage Checkpoint Inhibitor Psilostachyin C
The Journal of Organic Chemistry, 2011A concise total synthesis of the G2/M DNA damage checkpoint inhibitor psilostachyin C is reported using a 1,4-addition-aldol condensation-ring-closing metathesis (RCM) strategy. Initial biological studies indicate that psilostachyin C could enhance the sensitivity of the HeLa cell toward camptothecin (CPT) treatment via the activation of the caspase-3 ...
Chao, Li +6 more
openaire +2 more sources
BRCA1 regulates the G2/M checkpoint by activating Chk1 kinase upon DNA damage
Nature Genetics, 2002The breast cancer tumor-suppressor gene, BRCA1, encodes a protein with a BRCT domain-a motif that is found in many proteins that are implicated in DNA damage response and in genome stability. Phosphorylation of BRCA1 by the DNA damage-response proteins ATM, ATR and hCds1/Chk2 changes in response to DNA damage and at replication-block checkpoints ...
Ronit I, Yarden +4 more
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Serine–Threonine Kinase 38 regulates CDC25A stability and the DNA damage-induced G2/M checkpoint
Cellular Signalling, 2015Cells respond to DNA damage by activating protein kinase-mediated signaling pathways that promote cell-cycle arrest, DNA repair, or apoptosis. A key regulator of cell-cycle arrest is the CDC25A (cell division cycle 25 homologue A) phosphatase. CDC25A normally plays a pivotal role in regulating the G1/S and G2/M transitions by dephosphorylating and ...
Takemichi Fukasawa +2 more
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Environmental and Molecular Mutagenesis, 1999
Reactive oxygen species induce cellular damage and have been implicated as mediators for cellular signaling pathways. However, a linkage between the cellular redox status and cell cycle progression has not been demonstrated. We previously demonstrated, using the Chinese hamster ovary cell line AS52, that the cytotoxic and mutagenic effects of oxidative
G N, Bijur +3 more
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Reactive oxygen species induce cellular damage and have been implicated as mediators for cellular signaling pathways. However, a linkage between the cellular redox status and cell cycle progression has not been demonstrated. We previously demonstrated, using the Chinese hamster ovary cell line AS52, that the cytotoxic and mutagenic effects of oxidative
G N, Bijur +3 more
openaire +2 more sources
ΔNp73α compromises G2/M checkpoint inducing genomic instability in response to DNA damage
2015Deregulation of the cell cycle progression is a common feature of tumor cells and one of the driving forces in tumorigenesis, mostly by leading to unscheduled proliferation and genomic instability. The canonical p53 protein (p53α) and its relative p73 are shown to have various roles in cell cycle regulation in stress conditions, especially as a part of
Slade, Neda +2 more
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Breast Cancer Research and Treatment, 2010
Estrogen receptor beta (ERβ) inhibits proliferation in different cellular systems by regulating components of the cell cycle machinery. Eukaryotic cells respond to DNA damage by arresting in G1, S, or G2 phases of the cell cycle to initiate DNA repair. Most tumor cells due to disruptions in the p53-dependent G1 pathway are dependent on S-phase and G2/M
Christoforos G. Thomas +3 more
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Estrogen receptor beta (ERβ) inhibits proliferation in different cellular systems by regulating components of the cell cycle machinery. Eukaryotic cells respond to DNA damage by arresting in G1, S, or G2 phases of the cell cycle to initiate DNA repair. Most tumor cells due to disruptions in the p53-dependent G1 pathway are dependent on S-phase and G2/M
Christoforos G. Thomas +3 more
openaire +1 more source

