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Article: ATR dependent activation of Chk2

TitleATR dependent activation of Chk2
Authors
Issue Date2006
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31010
Citation
Journal Of Cellular Physiology, 2006, v. 208 n. 3, p. 613-619 How to Cite?
AbstractATM and ATR are essential regulators of DNA damage checkpoints in mammalian cells through their respective effectors, Chk2 and Chk1. Cross regulation of the ATM-Chk2 and ATR-Chk1 pathways is very limited, although ATM and ATR show overlapping function in a partnership and time-dependent manner. In this study, we report that Chk2 is a substrate of ATR in response to ionizing and ultraviolet radiation. ATR activation induced by ionizing radiation (IR) is weak in ATM+/+ cells. However, when ATM is inhibited by caffeine, ATR activation is markedly enhanced. Total Chk2 and Chk2 Thr68 are also hyperphosphorylated in the presence of caffeine. Both ATM+/+ and ATM-/- cells display normal ATR activation in response to UV radiation-induced DNA damage, which is caffeine sensitive. In two lines of ATM-deficient, as well as in an ATM siRNA silencing cell line, ATR is activated when the cells are exposed to IR and is able to phosphorylate Chk2 in vitro. These observations suggest that ATR is one of the kinases that is likely involved in phosphorylation of Chk2 in response to IR when ATM is deficient. © 2006 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/172916
ISSN
2015 Impact Factor: 4.155
2015 SCImago Journal Rankings: 1.842
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, XQen_US
dc.contributor.authorRedpath, JLen_US
dc.contributor.authorFan, STen_US
dc.contributor.authorStanbridge, EJen_US
dc.date.accessioned2012-10-30T06:25:47Z-
dc.date.available2012-10-30T06:25:47Z-
dc.date.issued2006en_US
dc.identifier.citationJournal Of Cellular Physiology, 2006, v. 208 n. 3, p. 613-619en_US
dc.identifier.issn0021-9541en_US
dc.identifier.urihttp://hdl.handle.net/10722/172916-
dc.description.abstractATM and ATR are essential regulators of DNA damage checkpoints in mammalian cells through their respective effectors, Chk2 and Chk1. Cross regulation of the ATM-Chk2 and ATR-Chk1 pathways is very limited, although ATM and ATR show overlapping function in a partnership and time-dependent manner. In this study, we report that Chk2 is a substrate of ATR in response to ionizing and ultraviolet radiation. ATR activation induced by ionizing radiation (IR) is weak in ATM+/+ cells. However, when ATM is inhibited by caffeine, ATR activation is markedly enhanced. Total Chk2 and Chk2 Thr68 are also hyperphosphorylated in the presence of caffeine. Both ATM+/+ and ATM-/- cells display normal ATR activation in response to UV radiation-induced DNA damage, which is caffeine sensitive. In two lines of ATM-deficient, as well as in an ATM siRNA silencing cell line, ATR is activated when the cells are exposed to IR and is able to phosphorylate Chk2 in vitro. These observations suggest that ATR is one of the kinases that is likely involved in phosphorylation of Chk2 in response to IR when ATM is deficient. © 2006 Wiley-Liss, Inc.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31010en_US
dc.relation.ispartofJournal of Cellular Physiologyen_US
dc.rightsJournal of Cellular Physiology. Copyright © John Wiley & Sons, Inc.-
dc.subject.meshCaffeine - Pharmacologyen_US
dc.subject.meshCell Cycle Proteins - Metabolism - Radiation Effectsen_US
dc.subject.meshCell Lineen_US
dc.subject.meshDna-Binding Proteins - Deficiency - Radiation Effectsen_US
dc.subject.meshEnzyme Activationen_US
dc.subject.meshFibroblastsen_US
dc.subject.meshHumansen_US
dc.subject.meshPhosphorylationen_US
dc.subject.meshProtein-Serine-Threonine Kinases - Deficiency - Metabolism - Radiation Effectsen_US
dc.subject.meshTumor Suppressor Proteins - Deficiency - Radiation Effectsen_US
dc.titleATR dependent activation of Chk2en_US
dc.typeArticleen_US
dc.identifier.emailWang, XQ: xqwang@hkucc.hku.hken_US
dc.identifier.emailFan, ST: stfan@hku.hken_US
dc.identifier.authorityWang, XQ=rp00507en_US
dc.identifier.authorityFan, ST=rp00355en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/jcp.20700en_US
dc.identifier.pmid16741947-
dc.identifier.scopuseid_2-s2.0-33746475848en_US
dc.identifier.hkuros135870-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33746475848&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume208en_US
dc.identifier.issue3en_US
dc.identifier.spage613en_US
dc.identifier.epage619en_US
dc.identifier.isiWOS:000239412300015-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWang, XQ=17343159900en_US
dc.identifier.scopusauthoridRedpath, JL=7006011559en_US
dc.identifier.scopusauthoridFan, ST=7402678224en_US
dc.identifier.scopusauthoridStanbridge, EJ=7103249410en_US

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