|
1
|
Biterge B and Schneider R: Histone variants: Key players of chromatin. Cell Tissue Res. 356:457–466. 2014.PubMed/NCBI View Article : Google Scholar
|
|
2
|
Luger K, Mäder AW, Richmond RK, Sargent DF and Richmond TJ: Crystal structure of the nucleosome core particle at 2.8 A resolution. Nature. 389:251–260. 1997.PubMed/NCBI View Article : Google Scholar
|
|
3
|
Singh RK, Paik J and Gunjan A: Generation and management of excess histones during the cell cycle. Front Biosci. 14:3145–3158. 2009.PubMed/NCBI View Article : Google Scholar
|
|
4
|
Redon C, Pilch D, Rogakou E, Sedelnikova O, Newrock K and Bonner W: Histone H2A variants H2AX and H2AZ. Curr Opin Genet Dev. 12:162–169. 2002.PubMed/NCBI View Article : Google Scholar
|
|
5
|
Kuo LJ and Yang LX: Gamma-H2AX - a novel biomarker for DNA double-strand breaks. In Vivo. 22:305–309. 2008.PubMed/NCBI
|
|
6
|
Sharma A, Singh K and Almasan A: Histone H2AX phosphorylation: A marker for DNA damage. Methods Mol Biol. 920:613–626. 2012.PubMed/NCBI View Article : Google Scholar
|
|
7
|
Varvara PV, Karaolanis G, Valavanis C, Stanc G, Tzaida O, Trihia H, Patapis P, Dimitroulis D and Perrea D: gamma-H2AX: A potential biomarker in breast cancer. Tumour Biol: Sep 25, 2019 (Epub ahead of print). doi: 10.1177/1010428319878536.
|
|
8
|
Johnson DP, Chandrasekharan MB, Dutreix M and Bhaskara S: Targeting DNA repair and chromatin crosstalk in cancer therapy. Cancers (Basel). 13(381)2021.PubMed/NCBI View Article : Google Scholar
|
|
9
|
Stiff T, O'Driscoll M, Rief N, Iwabuchi K, Löbrich M and Jeggo PA: ATM and DNA-PK function redundantly to phosphorylate H2AX after exposure to ionizing radiation. Cancer Res. 64:2390–2396. 2004.PubMed/NCBI View Article : Google Scholar
|
|
10
|
House NC, Koch MR and Freudenreich CH: Chromatin modifications and DNA repair: Beyond double-strand breaks. Front Genet. 5(296)2014.PubMed/NCBI View Article : Google Scholar
|
|
11
|
Ambekar SS, Hattur SS and Bule PB: DNA: Damage and repair mechanisms in humans. Glob J Pharm Pharm Sci. 3(555613)2018.
|
|
12
|
Rogakou EP, Boon C, Redon C and Bonner WM: Megabase chromatin domains involved in DNA double-strand breaks in vivo. J Cell Biol. 146:905–916. 1999.PubMed/NCBI View Article : Google Scholar
|
|
13
|
Osipov AN, Pustovalova M, Grekhova A, Eremin P, Vorobyova N, Pulin A, Zhavoronkov A, Roumiantsev S, Klokov DY and Eremin I: Low doses of X-rays induce prolonged and ATM-independent persistence of γH2AX foci in human gingival mesenchymal stem cells. Oncotarget. 6:27275–27287. 2015.PubMed/NCBI View Article : Google Scholar
|
|
14
|
Halicka HD, Huang X, Traganos F, King MA, Dai W and Darzynkiewicz Z: Histone H2AX phosphorylation after cell irradiation with UV-B: Relationship to cell cycle phase and induction of apoptosis. Cell Cycle. 4:339–345. 2005.PubMed/NCBI
|
|
15
|
Parsels LA, Parsels JD, Tanska DM, Maybaum J, Lawrence TS and Morgan MA: The contribution of DNA replication stress marked by high-intensity, pan-nuclear γH2AX staining to chemosensitization by CHK1 and WEE1 inhibitors. Cell Cycle. 17:1076–1086. 2018.PubMed/NCBI View Article : Google Scholar
|
|
16
|
Xiao H, Li TK, Yang J-M and Liu LF: Acidic pH induces topoisomerase II-mediated DNA damage. Proc Natl Acad Sci USA. 100:5205–5210. 2003.PubMed/NCBI View Article : Google Scholar
|
|
17
|
Kaneko H, Igarashi K, Kataoka K and Miura M: Heat shock induces phosphorylation of histone H2AX in mammalian cells. Biochem Biophys Res Commun. 328:1101–1106. 2005.PubMed/NCBI View Article : Google Scholar
|
|
18
|
Banáth JP and Olive PL: Expression of phosphorylated histone H2AX as a surrogate of cell killing by drugs that create DNA double-strand breaks. Cancer Res. 63:4347–4350. 2003.PubMed/NCBI
|
|
19
|
Kiziltepe T, Hideshima T, Catley L, Raje N, Yasui H, Shiraishi N, Okawa Y, Ikeda H, Vallet S, Pozzi S, et al: 5-Azacytidine, a DNA methyltransferase inhibitor, induces ATR-mediated DNA double-strand break responses, apoptosis, and synergistic cytotoxicity with doxorubicin and bortezomib against multiple myeloma cells. Mol Cancer Ther. 6:1718–1727. 2007.PubMed/NCBI View Article : Google Scholar
|
|
20
|
Guo Z, Kozlov S, Lavin MF, Person MD and Paull TT: ATM activation by oxidative stress. Science. 330:517–521. 2010.PubMed/NCBI View Article : Google Scholar
|
|
21
|
Li Z, Owonikoko TK, Sun SY, Ramalingam SS, Doetsch PW, Xiao ZQ, Khuri FR, Curran WJ and Deng X: c-Myc suppression of DNA double-strand break repair. Neoplasia. 14:1190–1202. 2012.PubMed/NCBI View Article : Google Scholar
|
|
22
|
Ewald B, Sampath D and Plunkett W: H2AX phosphorylation marks gemcitabine-induced stalled replication forks and their collapse upon S-phase checkpoint abrogation. Mol Cancer Ther. 6:1239–1248. 2007.PubMed/NCBI View Article : Google Scholar
|
|
23
|
Williamson J, Hughes CM, Burke G and Davison GW: A combined γ-H2AX and 53BP1 approach to determine the DNA damage-repair response to exercise in hypoxia. Free Radic Biol Med. 154:9–17. 2020.PubMed/NCBI View Article : Google Scholar
|
|
24
|
Sedelnikova OA, Horikawa I, Zimonjic DB, Popescu NC, Bonner WM and Barrett JC: Senescing human cells and ageing mice accumulate DNA lesions with unrepairable double-strand breaks. Nat Cell Biol. 6:168–170. 2004.PubMed/NCBI View Article : Google Scholar
|
|
25
|
Bekeschus S, Schütz CS, Niessner F, Wende K, Weltmann KD, Gelbrich N, von Woedtke T, Schmidt A and Stope MB: Elevated H2AX phosphorylation observed with kINPen plasma treatment is not caused by ROS-mediated DNA damage but is the consequence of apoptosis. Oxid Med Cell Longev. 2019(8535163)2019.PubMed/NCBI View Article : Google Scholar
|
|
26
|
Kulashreshtha M, Mehta IS, Kumar P and Rao BJ: Chromosome territory relocation during DNA repair requires nuclear myosin 1 recruitment to chromatin mediated by γ-H2AX signaling. Nucleic Acids Res. 44:8272–8291. 2016.PubMed/NCBI View Article : Google Scholar
|
|
27
|
Goutham HV, Mumbrekar KD, Vadhiraja BM, Fernandes DJ, Sharan K, Kanive Parashiva G, Kapaettu S and Bola Sadashiva SR: DNA double-strand break analysis by γ-H2AX foci: A useful method for determining the overreactors to radiation-induced acute reactions among head-and-neck cancer patients. Int J Radiat Oncol Biol Phys. 84:e607–e612. 2012.PubMed/NCBI View Article : Google Scholar
|
|
28
|
Sedelnikova OA, Rogakou EP, Panyutin IG and Bonner WM: Quantitative detection of (125)IdU-induced DNA double-strand breaks with gamma-H2AX antibody. Radiat Res. 158:486–492. 2002.PubMed/NCBI View Article : Google Scholar
|
|
29
|
Tomita M: Involvement of DNA-PK and ATM in radiation- and heat-induced DNA damage recognition and apoptotic cell death. J Radiat Res (Tokyo). 51:493–501. 2010.PubMed/NCBI View Article : Google Scholar
|
|
30
|
Fernandez-Capetillo O, Lee A, Nussenzweig M and Nussenzweig A: H2AX: The histone guardian of the genome. DNA Repair (Amst). 3:959–967. 2004.PubMed/NCBI View Article : Google Scholar
|
|
31
|
Li X, Nan A, Xiao Y, Chen Y and Lai Y: PP2A-B56є complex is involved in dephosphorylation of γ-H2AX in the repair process of CPT-induced DNA double-strand breaks. Toxicology. 331:57–65. 2015.PubMed/NCBI View Article : Google Scholar
|
|
32
|
Tu WZ, Li B, Huang B, Wang Y, Liu XD, Guan H, Zhang SM, Tang Y, Rang WQ and Zhou PK: γH2AX foci formation in the absence of DNA damage: Mitotic H2AX phosphorylation is mediated by the DNA-PKcs/CHK2 pathway. FEBS Lett. 587:3437–3443. 2013.PubMed/NCBI View Article : Google Scholar
|
|
33
|
Miller KM and Jackson SP: Histone marks: Repairing DNA breaks within the context of chromatin. Biochem Soc Trans. 40:370–376. 2012.PubMed/NCBI View Article : Google Scholar
|
|
34
|
Zhao H, Halicka HD, Garcia J, Li J and Darzynkiewicz Z: ATM activation and H2AX phosphorylation induced by genotoxic agents assessed by flow- and laser scanning cytometry. Methods Mol Biol. 1599:183–196. 2017.PubMed/NCBI View Article : Google Scholar
|
|
35
|
Hanasoge S and Ljungman M: H2AX phosphorylation after UV irradiation is triggered by DNA repair intermediates and is mediated by the ATR kinase. Carcinogenesis. 28:2298–2304. 2007.PubMed/NCBI View Article : Google Scholar
|
|
36
|
Park E-J, Chan DW, Park J-H, Oettinger MA and Kwon J: DNA-PK is activated by nucleosomes and phosphorylates H2AX within the nucleosomes in an acetylation-dependent manner. Nucleic Acids Res. 31:6819–6827. 2003.PubMed/NCBI View Article : Google Scholar
|
|
37
|
Kinner A, Wu W, Staudt C and Iliakis G: Gamma-H2AX in recognition and signaling of DNA double-strand breaks in the context of chromatin. Nucleic Acids Res. 36:5678–5694. 2008.PubMed/NCBI View Article : Google Scholar
|
|
38
|
Kim ST, Lim DS, Canman CE and Kastan MB: Substrate specificities and identification of putative substrates of ATM kinase family members. J Biol Chem. 274:37538–37543. 1999.PubMed/NCBI View Article : Google Scholar
|
|
39
|
Zhang F and Gong Z: Regulation of DNA double-strand break repair pathway choice: A new focus on 53BP1. J Zhejiang Univ Sci B. 22:38–46. 2021.PubMed/NCBI View Article : Google Scholar
|
|
40
|
Paull TT, Rogakou EP, Yamazaki V, Kirchgessner CU, Gellert M and Bonner WM: A critical role for histone H2AX in recruitment of repair factors to nuclear foci after DNA damage. Curr Biol. 10:886–895. 2000.PubMed/NCBI View Article : Google Scholar
|
|
41
|
Kang J, Ferguson D, Song H, Bassing C, Eckersdorff M, Alt FW and Xu Y: Functional interaction of H2AX, NBS1, and p53 in ATM-dependent DNA damage responses and tumor suppression. Mol Cell Biol. 25:661–670. 2005.PubMed/NCBI View Article : Google Scholar
|
|
42
|
Tanaka T, Huang X, Jorgensen E, Gietl D, Traganos F, Darzynkiewicz Z and Albino AP: ATM activation accompanies histone H2AX phosphorylation in A549 cells upon exposure to tobacco smoke. BMC Cell Biol. 8(26)2007.PubMed/NCBI View Article : Google Scholar
|
|
43
|
Watters GP, Smart DJ, Harvey JS and Austin CA: H2AX phosphorylation as a genotoxicity endpoint. Mutat Res. 679:50–58. 2009.PubMed/NCBI View Article : Google Scholar
|
|
44
|
Bartkova J, Horejsí Z, Koed K, Krämer A, Tort F, Zieger K, Guldberg P, Sehested M, Nesland JM, Lukas C, et al: DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis. Nature. 434:864–870. 2005.PubMed/NCBI View Article : Google Scholar
|
|
45
|
Olive PL and Banáth JP: Phosphorylation of histone H2AX as a measure of radiosensitivity. Int J Radiat Oncol Biol Phys. 58:331–335. 2004.PubMed/NCBI View Article : Google Scholar
|
|
46
|
Kawashima S, Kawaguchi N, Taniguchi K, Tashiro K, Komura K, Tanaka T, Inomata Y, Imai Y, Tanaka R, Yamamoto M, et al: γ-H2AX as a potential indicator of radiosensitivity in colorectal cancer cells. Oncol Lett. 20:2331–2337. 2020.PubMed/NCBI View Article : Google Scholar
|
|
47
|
Gorgoulis VG, Vassiliou L-VF, Karakaidos P, Zacharatos P, Kotsinas A, Liloglou T, Venere M, Ditullio RA Jr, Kastrinakis NG, Levy B, et al: Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions. Nature. 434:907–913. 2005.PubMed/NCBI View Article : Google Scholar
|
|
48
|
Palla VV, Karaolanis G, Katafigiotis I, Anastasiou I, Patapis P, Dimitroulis D and Perrea D: gamma-H2AX: Can it be established as a classical cancer prognostic factor? Tumour Biol: Mar 29, 2017 (Epub ahead of print). doi: 10.1177/1010428317695931.
|
|
49
|
Baritaud M, Cabon L, Delavallée L, Galán-Malo P, Gilles ME, Brunelle-Navas MN and Susin SA: AIF-mediated caspase-independent necroptosis requires ATM and DNA-PK-induced histone H2AX Ser139 phosphorylation. Cell Death Dis. 3(e390)2012.PubMed/NCBI View Article : Google Scholar
|
|
50
|
Mariotti LG, Pirovano G, Savage KI, Ghita M, Ottolenghi A, Prise KM and Schettino G: Use of the γ-H2AX assay to investigate DNA repair dynamics following multiple radiation exposures. PLoS One. 8(e79541)2013.PubMed/NCBI View Article : Google Scholar
|
