Detection of Histone H2AX Phosphorylation on Ser‐139 as an Indicator of DNA Damage

2019 ◽  
Vol 89 (1) ◽  
Author(s):  
Hong Zhao ◽  
Xuan Huang ◽  
H. Dorota Halicka ◽  
Zbigniew Darzynkiewicz
Keyword(s):  
Dna Damage ◽  
H2ax Phosphorylation ◽  
Histone H2ax ◽  
Histone H2ax Phosphorylation

scholarly journals Cytometry of ATM activation and histone H2AX phosphorylation to estimate extent of DNA damage induced by exogenous agents

2007 ◽  
Vol 71A (9) ◽  
pp. 648-661 ◽  
Author(s):  
Toshiki Tanaka ◽  
Xuan Huang ◽  
H. Dorota Halicka ◽  
Hong Zhao ◽  
Frank Traganos ◽  
...  
Keyword(s):  
Dna Damage ◽  
H2ax Phosphorylation ◽  
Histone H2ax ◽  
Exogenous Agents ◽  
Histone H2ax Phosphorylation

scholarly journals Constitutive Histone H2AX Phosphorylation and ATM Activation, the Reporters of DNA Damage by Endogenous Oxidants

Cell Cycle ◽  
2006 ◽  
Vol 5 (17) ◽  
pp. 1940-1945 ◽  
Author(s):  
Toshiki Tanaka ◽  
H. Dorota Halicka ◽  
Xuan Huang ◽  
Frank Traganos ◽  
Zbigniew Darzynkiewicz
Keyword(s):  
Dna Damage ◽  
H2ax Phosphorylation ◽  
Histone H2ax ◽  
Histone H2ax Phosphorylation

scholarly journals Role of intracellular calcium and NADPH oxidase NOX5-S in acid-induced DNA damage in Barrett's cells and Barrett's esophageal adenocarcinoma cells

2014 ◽  
Vol 306 (10) ◽  
pp. G863-G872 ◽  
Author(s):  
Dan Li ◽  
Weibiao Cao
Keyword(s):  
Dna Damage ◽  
Nadph Oxidase ◽  
Intracellular Calcium ◽  
Acid Treatment ◽  
Acid Reflux ◽  
Tail Moment ◽  
H2ax Phosphorylation ◽  
Histone H2ax ◽  
Intracellular Ca ◽  
Histone H2ax Phosphorylation

Mechanisms whereby acid reflux may accelerate the progression from Barrett's esophagus (BE) to esophageal adenocarcinoma (EA) are not fully understood. Acid and reactive oxygen species (ROS) have been reported to cause DNA damage in Barrett's cells. We have previously shown that NADPH oxidase NOX5-S is responsible for acid-induced H2O2 production in Barrett's cells and in EA cells. In this study we examined the role of intracellular calcium and NADPH oxidase NOX5-S in acid-induced DNA damage in a Barrett's EA cell line FLO and a Barrett's cell line CP-A. We found that pulsed acid treatment significantly increased tail moment in FLO and CP-A cells and histone H2AX phosphorylation in FLO cells. In addition, acid treatment significantly increased intracellular Ca2+ in FLO cells, an increase that is blocked by Ca2+-free medium with EGTA and thapsigargin. Acid-induced increase in tail moment was significantly decreased by NADPH oxidase inhibitor diphenylene iodonium in FLO cells, and by blockade of intracellular Ca2+ increase or knockdown of NOX5-S with NOX5 small-interfering RNA (siRNA) in FLO and CP-A cells. Acid-induced increase in histone H2AX phosphorylation was significantly decreased by NOX5 siRNA in FLO cells. Conversely, overexpression of NOX5-S significantly increased tail moment and histone H2AX phosphorylation in FLO cells. We conclude that pulsed acid treatment causes DNA damage via increase of intracellular calcium and activation of NOX5-S. It is possible that in BE acid reflux increases intracellular calcium, activates NOX5-S, and increases ROS production, which causes DNA damage, thereby contributing to the progression from BE to EA.

scholarly journals Critical Role of Monoubiquitination of Histone H2AX Protein in Histone H2AX Phosphorylation and DNA Damage Response

2011 ◽  
Vol 286 (35) ◽  
pp. 30806-30815 ◽  
Author(s):  
Ching-Yuan Wu ◽  
Hong-Yo Kang ◽  
Wei-Lei Yang ◽  
Juan Wu ◽  
Yun Seong Jeong ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Critical Role ◽  
H2ax Phosphorylation ◽  
Histone H2ax ◽  
Damage Response ◽  
Histone H2ax Phosphorylation
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