The Arf/p53 protein module, which induces apoptosis, down-regulates histone H2AX to allow normal cells to survive in the presence of anti-cancer drugs

Yuko Atsumi; Aki Inase; Tomoyuki Osawa; Eiji Sugihara; Ryo Sakasai; Hiroaki Fujimori; Hirobumi Teraoka; Hideyuki Saya; Masamoto Kanno; Fumio Tashiro; Hitoshi Nakagama; Mitsuko Masutani; Ken Ichi Yoshioka

doi:10.1074/jbc.M112.402560

The Arf/p53 protein module, which induces apoptosis, down-regulates histone H2AX to allow normal cells to survive in the presence of anti-cancer drugs

Yuko Atsumi
, Aki Inase
, Tomoyuki Osawa
, Eiji Sugihara
, Ryo Sakasai
, Hiroaki Fujimori
, Hirobumi Teraoka
, Hideyuki Saya
, Masamoto Kanno
, Fumio Tashiro
, Hitoshi Nakagama
, Mitsuko Masutani
, Ken Ichi Yoshioka

Research output: Contribution to journal › Article › peer-review

24 Citations (Scopus)

Abstract

Background: It is unclear how DNA-damaging agents target cancer cells over normal somatic cells. Results: Arf/p53-dependent down-regulation of H2AX enables normal cells to survive after DNA damage. Conclusion: Transformed cells, which harbor mutations in either Arf or p53, are more sensitive to DNA-damaging agents. Significance: Cellular transformation renders cells more susceptible to some DNA-damaging agents.

Original language	English
Pages (from-to)	13269-13277
Number of pages	9
Journal	Journal of Biological Chemistry
Volume	288
Issue number	19
DOIs	https://doi.org/10.1074/jbc.M112.402560
Publication status	Published - 10-05-2013
Externally published	Yes

All Science Journal Classification (ASJC) codes

Biochemistry
Molecular Biology
Cell Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1074/jbc.M112.402560

Cite this

Atsumi, Y., Inase, A., Osawa, T., Sugihara, E., Sakasai, R., Fujimori, H., Teraoka, H., Saya, H., Kanno, M., Tashiro, F., Nakagama, H., Masutani, M., & Yoshioka, K. I. (2013). The Arf/p53 protein module, which induces apoptosis, down-regulates histone H2AX to allow normal cells to survive in the presence of anti-cancer drugs. Journal of Biological Chemistry, 288(19), 13269-13277. https://doi.org/10.1074/jbc.M112.402560

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title = "The Arf/p53 protein module, which induces apoptosis, down-regulates histone H2AX to allow normal cells to survive in the presence of anti-cancer drugs",

abstract = "Background: It is unclear how DNA-damaging agents target cancer cells over normal somatic cells. Results: Arf/p53-dependent down-regulation of H2AX enables normal cells to survive after DNA damage. Conclusion: Transformed cells, which harbor mutations in either Arf or p53, are more sensitive to DNA-damaging agents. Significance: Cellular transformation renders cells more susceptible to some DNA-damaging agents.",

author = "Yuko Atsumi and Aki Inase and Tomoyuki Osawa and Eiji Sugihara and Ryo Sakasai and Hiroaki Fujimori and Hirobumi Teraoka and Hideyuki Saya and Masamoto Kanno and Fumio Tashiro and Hitoshi Nakagama and Mitsuko Masutani and Yoshioka, \{Ken Ichi\}",

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month = may,

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doi = "10.1074/jbc.M112.402560",

language = "English",

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Atsumi, Y, Inase, A, Osawa, T, Sugihara, E, Sakasai, R, Fujimori, H, Teraoka, H, Saya, H, Kanno, M, Tashiro, F, Nakagama, H, Masutani, M & Yoshioka, KI 2013, 'The Arf/p53 protein module, which induces apoptosis, down-regulates histone H2AX to allow normal cells to survive in the presence of anti-cancer drugs', Journal of Biological Chemistry, vol. 288, no. 19, pp. 13269-13277. https://doi.org/10.1074/jbc.M112.402560

TY - JOUR

T1 - The Arf/p53 protein module, which induces apoptosis, down-regulates histone H2AX to allow normal cells to survive in the presence of anti-cancer drugs

AU - Atsumi, Yuko

AU - Inase, Aki

AU - Osawa, Tomoyuki

AU - Sugihara, Eiji

AU - Sakasai, Ryo

AU - Fujimori, Hiroaki

AU - Teraoka, Hirobumi

AU - Saya, Hideyuki

AU - Kanno, Masamoto

AU - Tashiro, Fumio

AU - Nakagama, Hitoshi

AU - Masutani, Mitsuko

AU - Yoshioka, Ken Ichi

PY - 2013/5/10

Y1 - 2013/5/10

N2 - Background: It is unclear how DNA-damaging agents target cancer cells over normal somatic cells. Results: Arf/p53-dependent down-regulation of H2AX enables normal cells to survive after DNA damage. Conclusion: Transformed cells, which harbor mutations in either Arf or p53, are more sensitive to DNA-damaging agents. Significance: Cellular transformation renders cells more susceptible to some DNA-damaging agents.

AB - Background: It is unclear how DNA-damaging agents target cancer cells over normal somatic cells. Results: Arf/p53-dependent down-regulation of H2AX enables normal cells to survive after DNA damage. Conclusion: Transformed cells, which harbor mutations in either Arf or p53, are more sensitive to DNA-damaging agents. Significance: Cellular transformation renders cells more susceptible to some DNA-damaging agents.

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U2 - 10.1074/jbc.M112.402560

DO - 10.1074/jbc.M112.402560

M3 - Article

C2 - 23536184

AN - SCOPUS:84877707148

SN - 0021-9258

VL - 288

SP - 13269

EP - 13277

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

IS - 19

ER -

The Arf/p53 protein module, which induces apoptosis, down-regulates histone H2AX to allow normal cells to survive in the presence of anti-cancer drugs

Abstract

All Science Journal Classification (ASJC) codes

UN SDGs

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