Cyclin-Dependent Kinase 2–Dependent Phosphorylation of ATRIP Regulates the G2-M Checkpoint Response to DNA Damage [PDF]
Cancer Research, 2007 AbstractThe ATR-ATRIP kinase complex regulates cellular responses to DNA damage and replication stress. Mass spectrometry was used to identify phosphorylation sites on ATR and ATRIP to understand how the kinase complex is regulated by post-translational modifications.
Jeremy S. Myers +4 more
openalex +4 more sources
PLoS Biology, 2010 A combined computational and biochemical approach reveals how mitotic kinases allow cell division to proceed in the presence of DNA damage.
Marcel A.T.M. van Vugt +15 more
semanticscholar +5 more sources
BRCA1 Activates a G2-M Cell Cycle Checkpoint following 6-Thioguanine–Induced DNA Mismatch Damage [PDF]
Cancer Research, 2007 Abstract Human DNA mismatch repair (MMR) is involved in the response to certain chemotherapy drugs, including 6-thioguanine (6-TG). Consistently, MMR-deficient human tumor cells show resistance to 6-TG damage as manifested by a reduced G2-M arrest and decreased apoptosis.
Kazuhiko Yamane +2 more
openalex +4 more sources
Regulation of Saccharomyces Rad53 Checkpoint Kinase during Adaptation from DNA Damage–Induced G2/M Arrest [PDF]
Molecular Cell, 2001 Saccharomyces cells with one unrepaired double-strand break (DSB) adapt after checkpoint-mediated G2/M arrest. Adaptation is accompanied by loss of Rad53p checkpoint kinase activity and Chk1p phosphorylation. Rad53p kinase remains elevated in yku70delta and cdc5-ad cells that fail to adapt.
Achille Pellicioli +4 more
openalex +4 more sources
Oncogenic RAS Induces Accelerated Transition through G2/M and Promotes Defects in the G2 DNA Damage and Mitotic Spindle Checkpoints [PDF]
Journal of Biological Chemistry, 2005 Activating mutations of RAS are prevalent in thyroid follicular neoplasms, which commonly have chromosomal losses and gains. In thyroid cells, acute expression of HRAS(V12) increases the frequency of chromosomal abnormalities within one or two cell cycles, suggesting that RAS oncoproteins may interfere with cell cycle checkpoints required for ...
Jeffrey A. Knauf +5 more
openalex +3 more sources
Drosophila FMRP participates in the DNA damage response by regulating G2/M cell cycle checkpoint and apoptosis [PDF]
Human Molecular Genetics, 2012 Fragile X syndrome, the most common form of inherited mental retardation, is caused by the loss of the fragile X mental retardation protein (FMRP). FMRP is a ubiquitously expressed, multi-domain RNA-binding protein, but its in vivo function remains poorly understood.
Wei Liu +3 more
openalex +3 more sources
Oxidative stress-induced DNA damage of mouse zygotes triggers G2/M checkpoint and phosphorylates Cdc25 and Cdc2 [PDF]
Cell Stress and Chaperones, 2016 In vitro fertilized (IVF) embryos show both cell cycle and developmental arrest. We previously showed oxidative damage activates the ATM → Chk1 → Cdc25B/Cdc25C cascade to mediate G2/M cell cycle arrest for repair of hydrogen peroxide (H2O2)-induced oxidative damage in sperm.
Yuting Zhang +7 more
openalex +4 more sources
Ataxia Telangiectasia-mutated- and Rad3-related Protein Regulates the DNA Damage-induced G2/M Checkpoint through the Aurora A Cofactor Bora Protein [PDF]
Journal of Biological Chemistry, 2013 Polo-like kinase1 (Plk1) activation is inhibited in response to DNA damage, and this inhibition contributes to the activation of the G2/M checkpoint, although the molecular mechanism by which Plk1 is inhibited is not clear. Here we report that the DNA damage signaling pathway inhibits Plk1 activity through Bora.
Bo Qin +4 more
openalex +4 more sources
The cohesin complex is required for the DNA damage‐induced G2/M checkpoint in mammalian cells
The EMBO Journal, 2009 Cohesin complexes mediate sister chromatid cohesion. Cohesin also becomes enriched at DNA double-strand break sites and facilitates recombinational DNA repair. Here, we report that cohesin is essential for the DNA damage-induced G2/M checkpoint. In contrast to cohesin's role in DNA repair, the checkpoint function of cohesin is independent of its ...
Erwan Watrin, Jan‐Michael Peters
openalex +5 more sources
JS-K activates G2/M checkpoints through the DNA damage response and induces autophagy via CAMKKβ/AMPKα/mTOR pathway in bladder cancer cells [PDF]
Journal of Cancer, 2023 The aim of this study was to investigate the effects of JS-K, a nitric oxide donor prodrug, on DNA damage and autophagy in bladder cancer (BCa) cells and to explore the potential related mechanisms. Through detecting proliferation viability, cell morphology observation and colony formation assay low concentrations of JS-K significantly inhibited BCa ...
Yuwan Zhao +9 more
openalex +3 more sources