Epidermal Growth Factor Sensitizes Cells to Ionizing Radiation by Down-regulating Protein Mutated in Ataxia-Telangiectasia [PDF]
Journal of Biological Chemistry, 2001 Epidermal growth factor (EGF) has been reported to either sensitize or protect cells against ionizing radiation. We report here that EGF increases radiosensitivity in both human fibroblasts and lymphoblasts and down-regulates both ATM (mutated in ataxia-telangiectasia (A-T)) and the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs).
Nuri Gueven +7 more
openalex +4 more sources
Ataxia-Telangiectasia Mutated and the Mre11-Rad50-NBS1 Complex:Promising Targets for Radiosensitization [PDF]
, 2012 Radiotherapy plays a central part in cancer treatment, and use of radiosensitizing agents can greatly enhance this modality. Although studies have shown that several chemotherapeutic agents have the potential to increase the radiosensitivity of tumor ...
Fujiwara, Toshiyoshi +2 more
core +1 more source
Radiation-induced Assembly of Rad51 and Rad52 Recombination Complex Requires ATM and c-Abl [PDF]
, 1999 Cells from individuals with the recessive cancer-prone disorder ataxia telangiectasia (A-T) are hypersensitive to ionizing radiation (I-R). ATM (mutated in A-T) is a protein kinase whose activity is stimulated by I-R. c-Abl, a nonreceptor tyrosine kinase,
Arlinghaus, Ralph +14 more
core +1 more source
Supplementary Figure 2 from DNA Protein Kinase–Dependent G<sub>2</sub> Checkpoint Revealed following Knockdown of Ataxia-Telangiectasia Mutated in Human Mammary Epithelial Cells [PDF]
, 2023 Sonnet J.H. Arlander +3 more
openalex +2 more sources
MRE11 facilitates the removal of human topoisomerase II complexes from genomic DNA [PDF]
, 2012 Topoisomerase II creates a double-strand break intermediate with topoisomerase covalently coupled to the DNA via a 5'-phosphotyrosyl bond. These intermediate complexes can become cytotoxic protein-DNA adducts and DSB repair at these lesions requires ...
Austin, Caroline +10 more
core +3 more sources
Homeodomain Proteins Directly Regulate ATM Kinase Activity
Cell Reports, 2018 Summary: Ataxia-telangiectasia mutated (ATM) is a serine/threonine kinase that coordinates the response to DNA double-strand breaks and oxidative stress.
Tanya E. Johnson +8 more
doaj +1 more source
Antioxidants, 2023 Acetaminophen (APAP) is the major cause of drug-induced liver injury, with limited treatment options. APAP overdose invokes excessive oxidative stress that triggers mitochondria-to-nucleus retrograde pathways, contributing to APAP-induced liver injury ...
Yelei Cen +5 more
doaj +1 more source
Radiation induced DNA damage responses [PDF]
, 2006 The amazing feature of ionising radiation (IR) as a DNA damaging agent is the range of lesions it induces. Such lesions include base damage, single strand breaks (SSBs), double strand breaks (DSBs) of varying complexity and DNA cross links.
Jeggo, Penny, Löbrich, Markus
core +1 more source
Endogenous topoisomerase II-mediated DNA breaks drive thymic cancer predisposition linked to ATM deficiency [PDF]
, 2020 The ATM kinase is a master regulator of the DNA damage response to double-strand breaks (DSBs) and a well-established tumour suppressor whose loss is the cause of the neurodegenerative and cancer-prone syndrome Ataxia-Telangiectasia (A-T).
Bernal Lozano, Cristina +10 more
core +3 more sources
Chromosome breakage after G2 checkpoint release [PDF]
, 2006 DNA double-strand break (DSB) repair and checkpoint control represent distinct mechanisms to reduce chromosomal instability. Ataxia telangiectasia (A-T) cells have checkpoint arrest and DSB repair defects. We examine the efficiency and interplay of ATM's
Beucher, Andrea +8 more
core +4 more sources