DNA damage checkpoint control in cells exposed to ionizing radiation
Damage induced in the DNA after exposure of cells to ionizing radiation activates checkpoint pathways that inhibit progression of cells through the G1 and G2 phases and induce a transient delay in the progression through S phase. Checkpoints together with repair and apoptosis are integrated in a cir...
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| Veröffentlicht in: | Oncogene 2003-09, Vol.22 (37), p.5834-5847 |
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| container_title | Oncogene |
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| creator | Iliakis, George Wang, Ya Guan, Jun Wang, Huichen |
| description | Damage induced in the DNA after exposure of cells to ionizing radiation activates checkpoint pathways that inhibit progression of cells through the G1 and G2 phases and induce a transient delay in the progression through S phase. Checkpoints together with repair and apoptosis are integrated in a circuitry that determines the ultimate response of a cell to DNA damage. Checkpoint activation typically requires sensors and mediators of DNA damage, signal transducers and effectors. Here, we review the current state of knowledge regarding mechanisms of checkpoint activation and proteins involved in the different steps of the process. Emphasis is placed on the role of ATM and ATR, as well on CHK1 and CHK2 kinases in checkpoint response. The roles of downstream effectors, such as P53 and the CDC25 family of proteins, are also described, and connections between repair and checkpoint activation are attempted. The role of checkpoints in genomic stability and the potential of improving the treatment of cancer by DNA damage inducing agents through checkpoint abrogation are also briefly outlined. |
| doi_str_mv | 10.1038/sj.onc.1206682 |
| format | Article |
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Checkpoints together with repair and apoptosis are integrated in a circuitry that determines the ultimate response of a cell to DNA damage. Checkpoint activation typically requires sensors and mediators of DNA damage, signal transducers and effectors. Here, we review the current state of knowledge regarding mechanisms of checkpoint activation and proteins involved in the different steps of the process. Emphasis is placed on the role of ATM and ATR, as well on CHK1 and CHK2 kinases in checkpoint response. The roles of downstream effectors, such as P53 and the CDC25 family of proteins, are also described, and connections between repair and checkpoint activation are attempted. 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Checkpoints together with repair and apoptosis are integrated in a circuitry that determines the ultimate response of a cell to DNA damage. Checkpoint activation typically requires sensors and mediators of DNA damage, signal transducers and effectors. Here, we review the current state of knowledge regarding mechanisms of checkpoint activation and proteins involved in the different steps of the process. Emphasis is placed on the role of ATM and ATR, as well on CHK1 and CHK2 kinases in checkpoint response. The roles of downstream effectors, such as P53 and the CDC25 family of proteins, are also described, and connections between repair and checkpoint activation are attempted. The role of checkpoints in genomic stability and the potential of improving the treatment of cancer by DNA damage inducing agents through checkpoint abrogation are also briefly outlined.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Cancer</subject><subject>Cell Biology</subject><subject>Cell cycle</subject><subject>Cell Cycle - radiation effects</subject><subject>CHK1 protein</subject><subject>Cyclin-dependent kinases</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA damage</subject><subject>DNA Damage - radiation effects</subject><subject>DNA Repair</subject><subject>Genes, cdc - radiation effects</subject><subject>Genomes</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Ionizing radiation</subject><subject>Kinases</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Neoplasms - etiology</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - metabolism</subject><subject>Oncology</subject><subject>p53 Protein</subject><subject>Proteins</subject><subject>Radiation</subject><subject>review</subject><subject>S phase</subject><subject>Space life sciences</subject><subject>Surveillance</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFksuLFDEQxoMo7rh69ShBwVvP5tV5HIddX7DoRc8hk1SPGbuTMekB9a83zQ4MyC6SQ6jkV1VfJR9CLylZU8L1Vd2vc_JryoiUmj1CKyqU7PreiMdoRUxPOsM4u0DPat0TQpQh7Cm6oMwIxQ1ZoZubzxsc3OR2gP138D8OOaYZ-5zmkkccE_YwjhXDr0OuEPCcccwp_olph4sL0c0tfI6eDG6s8OK0X6Jv7999vf7Y3X758Ol6c9v5nom58yLIwaltAM8FKCW1EC2WmkOT5QZigINmiqkQtoMSmvbbgQeQfXC9D4xford3dQ8l_zxCne0U66LPJcjHahWXRDH9f5BqzXqhdQPf_APu87GkNoRlUlDOtBEL9fpBiikulJHyXGrnRrAxDXkuzi997YZqQ5UgaqHW91BtBZhie3UYYju_L8GXXGuBwR5KnFz5bSmxiwVs3dtmAXuyQEt4dRJ73E4QzvjpzxtwdQfUdpV2UM7TPFDyL0p8ug0</recordid><startdate>20030901</startdate><enddate>20030901</enddate><creator>Iliakis, George</creator><creator>Wang, Ya</creator><creator>Guan, Jun</creator><creator>Wang, Huichen</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20030901</creationdate><title>DNA damage checkpoint control in cells exposed to ionizing radiation</title><author>Iliakis, George ; Wang, Ya ; Guan, Jun ; Wang, Huichen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c524t-c4d6fa7bdec34e776844fa7683e902af09e3e82727ddbf74815bf3de65da5cd23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Cancer</topic><topic>Cell Biology</topic><topic>Cell cycle</topic><topic>Cell Cycle - radiation effects</topic><topic>CHK1 protein</topic><topic>Cyclin-dependent kinases</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA damage</topic><topic>DNA Damage - radiation effects</topic><topic>DNA Repair</topic><topic>Genes, cdc - radiation effects</topic><topic>Genomes</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Ionizing radiation</topic><topic>Kinases</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Neoplasms - etiology</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - metabolism</topic><topic>Oncology</topic><topic>p53 Protein</topic><topic>Proteins</topic><topic>Radiation</topic><topic>review</topic><topic>S phase</topic><topic>Space life sciences</topic><topic>Surveillance</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Iliakis, George</creatorcontrib><creatorcontrib>Wang, Ya</creatorcontrib><creatorcontrib>Guan, Jun</creatorcontrib><creatorcontrib>Wang, Huichen</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Iliakis, George</au><au>Wang, Ya</au><au>Guan, Jun</au><au>Wang, Huichen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DNA damage checkpoint control in cells exposed to ionizing radiation</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2003-09-01</date><risdate>2003</risdate><volume>22</volume><issue>37</issue><spage>5834</spage><epage>5847</epage><pages>5834-5847</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Damage induced in the DNA after exposure of cells to ionizing radiation activates checkpoint pathways that inhibit progression of cells through the G1 and G2 phases and induce a transient delay in the progression through S phase. Checkpoints together with repair and apoptosis are integrated in a circuitry that determines the ultimate response of a cell to DNA damage. Checkpoint activation typically requires sensors and mediators of DNA damage, signal transducers and effectors. Here, we review the current state of knowledge regarding mechanisms of checkpoint activation and proteins involved in the different steps of the process. Emphasis is placed on the role of ATM and ATR, as well on CHK1 and CHK2 kinases in checkpoint response. The roles of downstream effectors, such as P53 and the CDC25 family of proteins, are also described, and connections between repair and checkpoint activation are attempted. The role of checkpoints in genomic stability and the potential of improving the treatment of cancer by DNA damage inducing agents through checkpoint abrogation are also briefly outlined.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>12947390</pmid><doi>10.1038/sj.onc.1206682</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Springer Nature - Complete Springer Journals; Nature Journals Online; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Apoptosis Cancer Cell Biology Cell cycle Cell Cycle - radiation effects CHK1 protein Cyclin-dependent kinases Deoxyribonucleic acid DNA DNA damage DNA Damage - radiation effects DNA Repair Genes, cdc - radiation effects Genomes Human Genetics Humans Internal Medicine Ionizing radiation Kinases Medicine Medicine & Public Health Neoplasms - etiology Neoplasms - genetics Neoplasms - metabolism Oncology p53 Protein Proteins Radiation review S phase Space life sciences Surveillance |
| title | DNA damage checkpoint control in cells exposed to ionizing radiation |
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