Expression and Radiation-induced Phosphorylation of Histone H2AX in Mammalian Cells
Author(s) -
Kayo Yoshida,
Shuhei Yoshida,
Chikashi Shimoda,
Takashi Morita
Publication year - 2003
Publication title -
journal of radiation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.643
H-Index - 60
eISSN - 1349-9157
pISSN - 0449-3060
DOI - 10.1269/jrr.44.47
Subject(s) - histone , phosphorylation , ionizing radiation , dna damage , microbiology and biotechnology , genome instability , dna , biology , cell cycle , irradiation , chemistry , cell , biochemistry , physics , nuclear physics
The mouse histone H2AX (H2AX) has unique C-terminal Ser residues, which are phosphorylated in response to DNA double-strand breaks (DSBs) by ionizing radiation, suggesting that it plays a role in the maintenance of genomic stability. Here, we show that the H2AX protein was detected in most cells in various tissues, and was abundant in the S phase of the cell cycle. Following X-ray irradiation, H2AX was phosphorylated (gamma-H2AX) in the thymus, small intestine and testis. However, H2AX in epithelial cells in the villi of the small intestine were not strongly phosphorylated, even after X-irradiation. Thus, H2AX was expressed in almost all cells. However, the cells that expressed H2AX were not always phosphorylated by X-irradiation, suggesting a different mechanism of kination in those cells.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom