Open AccessNuclear Accumulation of p53 in Normal Human Fibroblasts Is Induced by Various Cellular Stresses which Evoke the Heat Shock Response, Independently of the Cell Cycle
Author(s) -
Sugano Tatsuo,
Nitta Makoto,
Ohmori Hiroyuki,
Yamaizumi Masaru
Publication year - 1995
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1995.tb03072.x
Subject(s) - puromycin , immunostaining , heat shock , cell cycle , shock (circulatory) , heat shock protein , microbiology and biotechnology , biology , dna damage , flow cytometry , cell , dna , biochemistry , protein biosynthesis , immunology , medicine , immunohistochemistry , gene
Nuclear accumulation of p53 is induced by various DNA damaging agents (the p53 response). Induction of nuclear accumulation of p53 after various cellular stresses, mostly other than DNA damage, including heat shock, was examined in normal human fibroblasts by immunostaining and flow cytometry using a mouse anti‐p53 monoclonal antibody. Immunostaining revealed nuclear accumulation of p53 within 6 h after various stresses [heat shock, osmotic shock, heavy metal (Cd), blockers of the cellular respiratory system (NaN 3 ), amino acid analogues (azetidine and canavanine), an inhibitor of protein synthesis (puromycin), and oxygen free radicals (H 2 O 2 )]. Heat shock proved to be one of the most effective inducers among these stresses. FACScan analysis revealed that this induction of p53 occurred regardless of the stage in the cell cycle and that accumulation of cells in G2/M occurred. As all of these stresses are known to induce the heat shock response, the mechanism of p53 induction after stresses and that of heat shock response may share, at least partly, some common signaling pathway(s).