Checking in on hypoxia/reoxygenation

Rachel A. Freiberg; Adam J. Krieg; Amato J. Giaccia; Ester M. Hammond

doi:10.4161/cc.5.12.2811

Checking in on hypoxia/reoxygenation

Rachel A. Freiberg
, Adam J. Krieg
, Amato J. Giaccia
, Ester M. Hammond

Research output: Contribution to journal › Review article › peer-review

24 Scopus citations

Abstract

Hypoxia/reoxygenation is a physiological stress that activates the DNA damage pathway. Significantly, this pathway is initiated during hypoxia, in the absence of detectable DNA damage. Our most recent study determined that during hypoxia, Chk 2 is phosphorylated in an ATM-dependent manner. In addition to this finding, we found that components of the MRN complex were not required for Chk 2 phosphorylation during hypoxia/reoxygenation. Once activated, Chk 2 initiates a signaling cascade, which induces a cell cycle arrest in the G₂ phase. Loss of the Chk 2-mediated arrest correlated with an increase in sensitivity to hypoxia/reoxygenation. In contrast, loss of a p53-mediated reoxygenation-induced G₁ arrest does not correlate with increased sensitivity to hypoxia/reoxygenation.

Original language	English (US)
Pages (from-to)	1304-1307
Number of pages	4
Journal	Cell Cycle
Volume	5
Issue number	12
DOIs	https://doi.org/10.4161/cc.5.12.2811
State	Published - Jun 15 2006
Externally published	Yes

Funding

We are grateful to both Michael Kastan and Grant Stewart for some of the cell lines used in this study. This work was supported by National Institutes of Health (NIH) grant CA88480 to A.J.G.

Funders	Funder number
Author National Institutes of Health National Institutes of Health National Institutes of Health National Institutes of Health The Bev Hartig Huntington's Disease Foundation National Institutes of Health
National Institute of Health-National Cancer Institute	R37CA088480

Keywords

ATM
Chk 2
Hypoxia
Reoxygenation

ASJC Scopus subject areas

Molecular Biology
Developmental Biology
Cell Biology

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10.4161/cc.5.12.2811

Cite this

@article{681dbe5adcc64b5d9172dbe2072ec348,

title = "Checking in on hypoxia/reoxygenation",

abstract = "Hypoxia/reoxygenation is a physiological stress that activates the DNA damage pathway. Significantly, this pathway is initiated during hypoxia, in the absence of detectable DNA damage. Our most recent study determined that during hypoxia, Chk 2 is phosphorylated in an ATM-dependent manner. In addition to this finding, we found that components of the MRN complex were not required for Chk 2 phosphorylation during hypoxia/reoxygenation. Once activated, Chk 2 initiates a signaling cascade, which induces a cell cycle arrest in the G2 phase. Loss of the Chk 2-mediated arrest correlated with an increase in sensitivity to hypoxia/reoxygenation. In contrast, loss of a p53-mediated reoxygenation-induced G1 arrest does not correlate with increased sensitivity to hypoxia/reoxygenation.",

keywords = "ATM, Chk 2, Hypoxia, Reoxygenation",

author = "Freiberg, \{Rachel A.\} and Krieg, \{Adam J.\} and Giaccia, \{Amato J.\} and Hammond, \{Ester M.\}",

note = "Funding Information: We are grateful to both Michael Kastan and Grant Stewart for some of the cell lines used in this study. This work was supported by National Institutes of Health (NIH) grant CA88480 to A.J.G.",

year = "2006",

month = jun,

day = "15",

doi = "10.4161/cc.5.12.2811",

language = "English (US)",

volume = "5",

pages = "1304--1307",

journal = "Cell Cycle",

issn = "1538-4101",

publisher = "Taylor and Francis Ltd.",

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}

TY - JOUR

T1 - Checking in on hypoxia/reoxygenation

AU - Freiberg, Rachel A.

AU - Krieg, Adam J.

AU - Giaccia, Amato J.

AU - Hammond, Ester M.

N1 - Funding Information: We are grateful to both Michael Kastan and Grant Stewart for some of the cell lines used in this study. This work was supported by National Institutes of Health (NIH) grant CA88480 to A.J.G.

PY - 2006/6/15

Y1 - 2006/6/15

N2 - Hypoxia/reoxygenation is a physiological stress that activates the DNA damage pathway. Significantly, this pathway is initiated during hypoxia, in the absence of detectable DNA damage. Our most recent study determined that during hypoxia, Chk 2 is phosphorylated in an ATM-dependent manner. In addition to this finding, we found that components of the MRN complex were not required for Chk 2 phosphorylation during hypoxia/reoxygenation. Once activated, Chk 2 initiates a signaling cascade, which induces a cell cycle arrest in the G2 phase. Loss of the Chk 2-mediated arrest correlated with an increase in sensitivity to hypoxia/reoxygenation. In contrast, loss of a p53-mediated reoxygenation-induced G1 arrest does not correlate with increased sensitivity to hypoxia/reoxygenation.

AB - Hypoxia/reoxygenation is a physiological stress that activates the DNA damage pathway. Significantly, this pathway is initiated during hypoxia, in the absence of detectable DNA damage. Our most recent study determined that during hypoxia, Chk 2 is phosphorylated in an ATM-dependent manner. In addition to this finding, we found that components of the MRN complex were not required for Chk 2 phosphorylation during hypoxia/reoxygenation. Once activated, Chk 2 initiates a signaling cascade, which induces a cell cycle arrest in the G2 phase. Loss of the Chk 2-mediated arrest correlated with an increase in sensitivity to hypoxia/reoxygenation. In contrast, loss of a p53-mediated reoxygenation-induced G1 arrest does not correlate with increased sensitivity to hypoxia/reoxygenation.

KW - ATM

KW - Chk 2

KW - Hypoxia

KW - Reoxygenation

UR - https://www.scopus.com/pages/publications/33745148690

UR - https://www.scopus.com/pages/publications/33745148690#tab=citedBy

U2 - 10.4161/cc.5.12.2811

DO - 10.4161/cc.5.12.2811

M3 - Review article

C2 - 16760660

AN - SCOPUS:33745148690

SN - 1538-4101

VL - 5

SP - 1304

EP - 1307

JO - Cell Cycle

JF - Cell Cycle

IS - 12

ER -

Checking in on hypoxia/reoxygenation

Abstract

Funding

Keywords

ASJC Scopus subject areas

Access to Document

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