Results 221 to 230 of about 39,406 (258)

Serine–Threonine Kinase 38 regulates CDC25A stability and the DNA damage-induced G2/M checkpoint

open access: closedCellular Signalling, 2015
Cells 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
openalex   +3 more sources

ΔNp73α compromises G2/M checkpoint inducing genomic instability in response to DNA damage

open access: closed, 2015
Deregulation 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
Anđela Horvat   +3 more
  +4 more sources

Estrogen receptor beta decreases survival of p53-defective cancer cells after DNA damage by impairing G2/M checkpoint signaling

open access: closedBreast 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 Thomas   +3 more
openalex   +2 more sources

374: c-Abl tyrosine kinase regulates recovery from the G2-M DNA damage induced checkpoint

open access: closedEuropean Journal of Cancer, 2014
V Meltser, Nina Reuven, Yoav D. Shaul
openalex   +2 more sources
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DNA damage checkpoint kinases in cancer

Expert Reviews in Molecular Medicine, 2020
DNA damage response (DDR) pathway prevents high level endogenous and environmental DNA damage being replicated and passed on to the next generation of cells via an orchestrated and integrated network of cell cycle checkpoint signalling and DNA repair ...
Hannah L. Smith   +3 more
semanticscholar   +1 more source

PARP-1 inhibitor sensitizes arsenic trioxide in hepatocellular carcinoma cells via abrogation of G2/M checkpoint and suppression of DNA damage repair

Chemico-Biological Interactions, 2015
Arsenic trioxide (ATO) is successfully used to treat hematological malignancies. However, the clinical application of the agent in solid tumors is largely limited by its dose-dependent toxicity which results from the high intrinsic resistance of the cancer cells.
Qingying, Luo   +3 more
openaire   +2 more sources

Radiation therapy‐associated toxicity: Etiology, management, and prevention

Ca-A Cancer Journal for Clinicians, 2021
Kyle Wang
exaly  

Female erectile tissues and sexual dysfunction after pelvic radiotherapy: A scoping review

Ca-A Cancer Journal for Clinicians, 2022
Deborah C Marshall, Mas   +2 more
exaly  

Antibiotic-induced collateral damage to the microbiota and associated infections

Nature Reviews Microbiology, 2023
Laura de Nies   +2 more
exaly  

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