Nitric Oxide: Genomic Instability And Synthetic Lethality
نویسندگان
چکیده
منابع مشابه
Combining ATR suppression with oncogenic Ras synergistically increases genomic instability, causing synthetic lethality or tumorigenesis in a dosage-dependent manner.
Previous studies indicate that oncogenic stress activates the ATR-Chk1 pathway. Here, we show that ATR-Chk1 pathway engagement is essential for limiting genomic instability following oncogenic Ras transformation. ATR pathway inhibition in combination with oncogenic Ras expression synergistically increased genomic instability, as quantified by chromatid breaks, sister chromatid exchanges, and H2...
متن کاملNitric oxide and the bioactivities
Nitric oxide (NO), previously known as Endothelium-Derived Relaxing Factor (EDRF) is involved in a wide range of physiological and pathophysiological mechanisms. It is synthesized endogenously by the enzymes Nitric Oxide Synthase (NOS) in specialized tissues from its precursor L-arginine, yielding L-citrulline as a byproduct. It is released by a family of isoenzymes, viz., the endothelial (eNOS...
متن کاملNitric oxide and the bioactivities
Nitric oxide (NO), previously known as Endothelium-Derived Relaxing Factor (EDRF) is involved in a wide range of physiological and pathophysiological mechanisms. It is synthesized endogenously by the enzymes Nitric Oxide Synthase (NOS) in specialized tissues from its precursor L-arginine, yielding L-citrulline as a byproduct. It is released by a family of isoenzymes, viz., the endothelial (eNOS...
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Ataxia telangiectasia (A-T) mutated (ATM) kinase orchestrates deoxyribonucleic acid (DNA) damage responses by phosphorylating numerous substrates implicated in DNA repair and cell cycle checkpoint activation. A-T patients and mouse models that express no ATM protein undergo normal embryonic development but exhibit pleiotropic DNA repair defects. In this paper, we report that mice carrying homoz...
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ژورنال
عنوان ژورنال: Redox Biology
سال: 2015
ISSN: 2213-2317
DOI: 10.1016/j.redox.2015.09.013