Take your PIKK: tumour viruses and DNA damage response pathways
Viruses regulate cellular processes to facilitate viral replication. Manipulation of nuclear proteins and pathways by nuclear replicating viruses often causes cellular genome instability that contributes to transformation. The cellular DNA damage response (DDR) safeguards the host to maintain genome...
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| Veröffentlicht in: | Philosophical transactions of the Royal Society of London. Series B. Biological sciences 2017-10, Vol.372 (1732), p.20160269-20160269 |
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| container_issue | 1732 |
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| container_title | Philosophical transactions of the Royal Society of London. Series B. Biological sciences |
| container_volume | 372 |
| creator | Pancholi, Neha J. Price, Alexander M. Weitzman, Matthew D. |
| description | Viruses regulate cellular processes to facilitate viral replication. Manipulation of nuclear proteins and pathways by nuclear replicating viruses often causes cellular genome instability that contributes to transformation. The cellular DNA damage response (DDR) safeguards the host to maintain genome integrity, but DNA tumour viruses can manipulate the DDR to promote viral propagation. In this review, we describe the interactions of DNA tumour viruses with the phosphatidylinositol 3-kinase-like protein kinase (PIKK) pathways, which are central regulatory arms of the DDR. We review how signalling through the ataxia telangiectasia mutated (ATM), ataxia telangiectasia and Rad3 related (ATR), and DNA-dependent protein kinases (DNA-PK) influences viral life cycles, and how their manipulation by viral proteins may contribute to tumour formation.
This article is part of the themed issue ‘Human oncogenic viruses’. |
| doi_str_mv | 10.1098/rstb.2016.0269 |
| format | Article |
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This article is part of the themed issue ‘Human oncogenic viruses’.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Ataxia</subject><subject>Ataxia telangiectasia mutated protein</subject><subject>Ataxia Telangiectasia Mutated Proteins - physiology</subject><subject>Carcinogenesis - genetics</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Damage</subject><subject>Dna Damage Response</subject><subject>DNA Repair</subject><subject>DNA Tumor Viruses - physiology</subject><subject>DNA viruses</subject><subject>DNA-Activated Protein Kinase - physiology</subject><subject>DNA-dependent protein kinase</subject><subject>Genetic transformation</subject><subject>Genomes</subject><subject>Genomic instability</subject><subject>Humans</subject><subject>Kinases</subject><subject>Life cycles</subject><subject>Pikk</subject><subject>Protein kinase</subject><subject>Protein Kinases</subject><subject>Proteins</subject><subject>Replication</subject><subject>Review</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Stability</subject><subject>Tumor viruses</subject><subject>Tumors</subject><subject>Tumour Virus</subject><subject>Viral Proteins - metabolism</subject><subject>Viruses</subject><issn>0962-8436</issn><issn>1471-2970</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc1v1DAQxS0EosvClSOKxIVLtrYn6w8OVKWlpWoFCJazZcdO63bzgZ1sFf76OmwpFAQn25qf582bh9BzghcES7EbYm8WFBO2wJTJB2hGCk5yKjl-iGZYMpqLAtgOehLjJcZYLnnxGO1QISRIYDO0t9JXLhvbIWSfTk5PX2f9UE-PjQ9DdDHTjc0OP-xnVtf63GXBxa5toss63V9c6zE-RY8qvY7u2e05R1-P3q0O3udnH49PDvbP8nLJaJ_rAnMKzEBhhawwsaLSQMoSmBTGVFpyaUsjSGGKylpsmYWKF4ZZAxxkZWCO3mz7doOpnS1d0we9Vl3wtQ6jarVX9yuNv1Dn7UYtl5JzYKnBq9sGof02uNir2sfSrde6ce0QFZEg0h6hEAl9-Qd6mVbSJHuJEpB2R5OZOVpsqTK0MQZX3Q1DsJqyUVM2aspGTdmkDy9-t3CH_wwjAVdbILRjEmtL7_rxl_bnL6u3G-DUEw5UYQEEcwLp-t13W61UVD7GwakfyH39v8eB_6n9w8QNe8y_UA</recordid><startdate>20171019</startdate><enddate>20171019</enddate><creator>Pancholi, Neha J.</creator><creator>Price, Alexander M.</creator><creator>Weitzman, Matthew D.</creator><general>The Royal Society</general><general>The Royal Society Publishing</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>7QG</scope><scope>7QP</scope><scope>7SN</scope><scope>7SS</scope><scope>7TK</scope><scope>C1K</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9713-167X</orcidid></search><sort><creationdate>20171019</creationdate><title>Take your PIKK: tumour viruses and DNA damage response pathways</title><author>Pancholi, Neha J. ; Price, Alexander M. ; Weitzman, Matthew D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c562t-a407236b34d89f01d8fa31cc3698bbfa979dcb814b4fdd0d6d3f74b6db3739fb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Ataxia</topic><topic>Ataxia telangiectasia mutated protein</topic><topic>Ataxia Telangiectasia Mutated Proteins - physiology</topic><topic>Carcinogenesis - genetics</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA Damage</topic><topic>Dna Damage Response</topic><topic>DNA Repair</topic><topic>DNA Tumor Viruses - physiology</topic><topic>DNA viruses</topic><topic>DNA-Activated Protein Kinase - physiology</topic><topic>DNA-dependent protein kinase</topic><topic>Genetic transformation</topic><topic>Genomes</topic><topic>Genomic instability</topic><topic>Humans</topic><topic>Kinases</topic><topic>Life cycles</topic><topic>Pikk</topic><topic>Protein kinase</topic><topic>Protein Kinases</topic><topic>Proteins</topic><topic>Replication</topic><topic>Review</topic><topic>Signal Transduction</topic><topic>Signaling</topic><topic>Stability</topic><topic>Tumor viruses</topic><topic>Tumors</topic><topic>Tumour Virus</topic><topic>Viral Proteins - metabolism</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pancholi, Neha J.</creatorcontrib><creatorcontrib>Price, Alexander M.</creatorcontrib><creatorcontrib>Weitzman, Matthew D.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Philosophical transactions of the Royal Society of London. Series B. Biological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pancholi, Neha J.</au><au>Price, Alexander M.</au><au>Weitzman, Matthew D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Take your PIKK: tumour viruses and DNA damage response pathways</atitle><jtitle>Philosophical transactions of the Royal Society of London. Series B. Biological sciences</jtitle><stitle>Phil. Trans. R. Soc. B</stitle><addtitle>Philos Trans R Soc Lond B Biol Sci</addtitle><date>2017-10-19</date><risdate>2017</risdate><volume>372</volume><issue>1732</issue><spage>20160269</spage><epage>20160269</epage><pages>20160269-20160269</pages><issn>0962-8436</issn><eissn>1471-2970</eissn><abstract>Viruses regulate cellular processes to facilitate viral replication. Manipulation of nuclear proteins and pathways by nuclear replicating viruses often causes cellular genome instability that contributes to transformation. The cellular DNA damage response (DDR) safeguards the host to maintain genome integrity, but DNA tumour viruses can manipulate the DDR to promote viral propagation. In this review, we describe the interactions of DNA tumour viruses with the phosphatidylinositol 3-kinase-like protein kinase (PIKK) pathways, which are central regulatory arms of the DDR. We review how signalling through the ataxia telangiectasia mutated (ATM), ataxia telangiectasia and Rad3 related (ATR), and DNA-dependent protein kinases (DNA-PK) influences viral life cycles, and how their manipulation by viral proteins may contribute to tumour formation.
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| ispartof | Philosophical transactions of the Royal Society of London. Series B. Biological sciences, 2017-10, Vol.372 (1732), p.20160269-20160269 |
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| subjects | 1-Phosphatidylinositol 3-kinase Ataxia Ataxia telangiectasia mutated protein Ataxia Telangiectasia Mutated Proteins - physiology Carcinogenesis - genetics Deoxyribonucleic acid DNA DNA Damage Dna Damage Response DNA Repair DNA Tumor Viruses - physiology DNA viruses DNA-Activated Protein Kinase - physiology DNA-dependent protein kinase Genetic transformation Genomes Genomic instability Humans Kinases Life cycles Pikk Protein kinase Protein Kinases Proteins Replication Review Signal Transduction Signaling Stability Tumor viruses Tumors Tumour Virus Viral Proteins - metabolism Viruses |
| title | Take your PIKK: tumour viruses and DNA damage response pathways |
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