p400 Is Required for E1A to Promote Apoptosis
The adenovirus E1A oncoprotein promotes proliferation and transformation by binding cellular proteins, including members of the retinoblastoma protein family, the p300/CREB-binding protein transcriptional coactivators, and the p400-TRRAP chromatin-remodeling complex. E1A also promotes apoptosis, in...
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| Veröffentlicht in: | The Journal of biological chemistry 2005-06, Vol.280 (23), p.21915-21923 |
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| container_title | The Journal of biological chemistry |
| container_volume | 280 |
| creator | Samuelson, Andrew V. Narita, Masako Chan, Ho-Man Jin, Jianping de Stanchina, Elisa McCurrach, Mila E. Narita, Masashi Fuchs, Miriam Livingston, David M. Lowe, Scott W. |
| description | The adenovirus E1A oncoprotein promotes proliferation and transformation by binding cellular proteins, including members of the retinoblastoma protein family, the p300/CREB-binding protein transcriptional coactivators, and the p400-TRRAP chromatin-remodeling complex. E1A also promotes apoptosis, in part, by engaging the ARF-p53 tumor suppressor pathway. We show that E1A induces ARF and p53 and promotes apoptosis in normal fibroblasts by physically associating with the retinoblastoma protein and a p400-TRRAP complex and that its interaction with p300 is largely dispensable for these effects. We further show that E1A increases p400 expression and, conversely, that suppression of p400 using stable RNA interference reduces the levels of ARF, p53, and apoptosis in E1A-expressing cells. Therefore, whereas E1A inactivates the retinoblastoma protein, it requires p400 to efficiently promote cell death. These results identify p400 as a regulator of the ARF-p53 pathway and a component of the cellular machinery that couples proliferation to cell death. |
| doi_str_mv | 10.1074/jbc.M414564200 |
| format | Article |
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E1A also promotes apoptosis, in part, by engaging the ARF-p53 tumor suppressor pathway. We show that E1A induces ARF and p53 and promotes apoptosis in normal fibroblasts by physically associating with the retinoblastoma protein and a p400-TRRAP complex and that its interaction with p300 is largely dispensable for these effects. We further show that E1A increases p400 expression and, conversely, that suppression of p400 using stable RNA interference reduces the levels of ARF, p53, and apoptosis in E1A-expressing cells. Therefore, whereas E1A inactivates the retinoblastoma protein, it requires p400 to efficiently promote cell death. These results identify p400 as a regulator of the ARF-p53 pathway and a component of the cellular machinery that couples proliferation to cell death.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M414564200</identifier><identifier>PMID: 15741165</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adenovirus ; Adenovirus E1A Proteins - metabolism ; Adenovirus E1A Proteins - physiology ; ADP-Ribosylation Factors - metabolism ; Animals ; Apoptosis ; Binding Sites ; Blotting, Northern ; Blotting, Western ; Cell Line ; Cell Survival ; Chromatin - metabolism ; DNA Helicases - metabolism ; DNA Helicases - physiology ; DNA-Binding Proteins - metabolism ; DNA-Binding Proteins - physiology ; Dose-Response Relationship, Drug ; Doxorubicin - pharmacology ; E1A-Associated p300 Protein ; Fibroblasts - metabolism ; Gene Deletion ; Gene Expression Regulation ; Gene Transfer Techniques ; Genetic Vectors ; Humans ; Immunoblotting ; Immunoprecipitation ; Mice ; Microscopy, Fluorescence ; Mutation ; Nuclear Proteins - metabolism ; Protein Binding ; Protein Structure, Tertiary ; Retinoblastoma Protein - metabolism ; Retroviridae - genetics ; RNA Interference ; Structure-Activity Relationship ; Trans-Activators - metabolism ; Transcriptional Activation ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>The Journal of biological chemistry, 2005-06, Vol.280 (23), p.21915-21923</ispartof><rights>2005 © 2005 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-96e167079a7beb8e80c16ca2f585fe443e052f577156de588421c6eb58c922b03</citedby><cites>FETCH-LOGICAL-c442t-96e167079a7beb8e80c16ca2f585fe443e052f577156de588421c6eb58c922b03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15741165$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Samuelson, Andrew V.</creatorcontrib><creatorcontrib>Narita, Masako</creatorcontrib><creatorcontrib>Chan, Ho-Man</creatorcontrib><creatorcontrib>Jin, Jianping</creatorcontrib><creatorcontrib>de Stanchina, Elisa</creatorcontrib><creatorcontrib>McCurrach, Mila E.</creatorcontrib><creatorcontrib>Narita, Masashi</creatorcontrib><creatorcontrib>Fuchs, Miriam</creatorcontrib><creatorcontrib>Livingston, David M.</creatorcontrib><creatorcontrib>Lowe, Scott W.</creatorcontrib><title>p400 Is Required for E1A to Promote Apoptosis</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>The adenovirus E1A oncoprotein promotes proliferation and transformation by binding cellular proteins, including members of the retinoblastoma protein family, the p300/CREB-binding protein transcriptional coactivators, and the p400-TRRAP chromatin-remodeling complex. 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These results identify p400 as a regulator of the ARF-p53 pathway and a component of the cellular machinery that couples proliferation to cell death.</description><subject>Adenovirus</subject><subject>Adenovirus E1A Proteins - metabolism</subject><subject>Adenovirus E1A Proteins - physiology</subject><subject>ADP-Ribosylation Factors - metabolism</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Binding Sites</subject><subject>Blotting, Northern</subject><subject>Blotting, Western</subject><subject>Cell Line</subject><subject>Cell Survival</subject><subject>Chromatin - metabolism</subject><subject>DNA Helicases - metabolism</subject><subject>DNA Helicases - physiology</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>DNA-Binding Proteins - physiology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Doxorubicin - pharmacology</subject><subject>E1A-Associated p300 Protein</subject><subject>Fibroblasts - metabolism</subject><subject>Gene Deletion</subject><subject>Gene Expression Regulation</subject><subject>Gene Transfer Techniques</subject><subject>Genetic Vectors</subject><subject>Humans</subject><subject>Immunoblotting</subject><subject>Immunoprecipitation</subject><subject>Mice</subject><subject>Microscopy, Fluorescence</subject><subject>Mutation</subject><subject>Nuclear Proteins - metabolism</subject><subject>Protein Binding</subject><subject>Protein Structure, Tertiary</subject><subject>Retinoblastoma Protein - metabolism</subject><subject>Retroviridae - genetics</subject><subject>RNA Interference</subject><subject>Structure-Activity Relationship</subject><subject>Trans-Activators - metabolism</subject><subject>Transcriptional Activation</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMFLwzAUh4Mobk6vHqUH8daZlyZNehwydTBRRMFbaNNXl7EuNekU_3szNtjJd3k8-H4_Hh8hl0DHQCW_XVZm_MSBi5wzSo_IEKjK0kzAxzEZUsogLZhQA3IWwpLG4QWckgEIyQFyMSRpxylNZiF5xa-N9VgnjfPJFCZJ75IX71rXYzLpXNe7YMM5OWnKVcCL_R6R9_vp291jOn9-mN1N5qnhnPVpkSPkksqilBVWChU1kJuSNUKJBjnPkIp4SAkir1EoxRmYHCuhTMFYRbMRudn1dt59bTD0urXB4GpVrtFtggYpOM8lj-B4BxrvQvDY6M7btvS_GqjeCtJRkD4IioGrffOmarE-4HsjEbjeAQv7ufiJRnRlnVlgq5mimmWaQQFbTO0wjBq-LXodjMW1wTpGTK9rZ_974Q9GQnxQ</recordid><startdate>20050610</startdate><enddate>20050610</enddate><creator>Samuelson, Andrew V.</creator><creator>Narita, Masako</creator><creator>Chan, Ho-Man</creator><creator>Jin, Jianping</creator><creator>de Stanchina, Elisa</creator><creator>McCurrach, Mila E.</creator><creator>Narita, Masashi</creator><creator>Fuchs, Miriam</creator><creator>Livingston, David M.</creator><creator>Lowe, Scott W.</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</general><scope>6I.</scope><scope>AAFTH</scope><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>7TM</scope></search><sort><creationdate>20050610</creationdate><title>p400 Is Required for E1A to Promote Apoptosis</title><author>Samuelson, Andrew V. ; Narita, Masako ; Chan, Ho-Man ; Jin, Jianping ; de Stanchina, Elisa ; McCurrach, Mila E. ; Narita, Masashi ; Fuchs, Miriam ; Livingston, David M. ; Lowe, Scott W.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-96e167079a7beb8e80c16ca2f585fe443e052f577156de588421c6eb58c922b03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adenovirus</topic><topic>Adenovirus E1A Proteins - metabolism</topic><topic>Adenovirus E1A Proteins - physiology</topic><topic>ADP-Ribosylation Factors - metabolism</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Binding Sites</topic><topic>Blotting, Northern</topic><topic>Blotting, Western</topic><topic>Cell Line</topic><topic>Cell Survival</topic><topic>Chromatin - metabolism</topic><topic>DNA Helicases - metabolism</topic><topic>DNA Helicases - physiology</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>DNA-Binding Proteins - physiology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Doxorubicin - pharmacology</topic><topic>E1A-Associated p300 Protein</topic><topic>Fibroblasts - metabolism</topic><topic>Gene Deletion</topic><topic>Gene Expression Regulation</topic><topic>Gene Transfer Techniques</topic><topic>Genetic Vectors</topic><topic>Humans</topic><topic>Immunoblotting</topic><topic>Immunoprecipitation</topic><topic>Mice</topic><topic>Microscopy, Fluorescence</topic><topic>Mutation</topic><topic>Nuclear Proteins - metabolism</topic><topic>Protein Binding</topic><topic>Protein Structure, Tertiary</topic><topic>Retinoblastoma Protein - metabolism</topic><topic>Retroviridae - genetics</topic><topic>RNA Interference</topic><topic>Structure-Activity Relationship</topic><topic>Trans-Activators - metabolism</topic><topic>Transcriptional Activation</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Samuelson, Andrew V.</creatorcontrib><creatorcontrib>Narita, Masako</creatorcontrib><creatorcontrib>Chan, Ho-Man</creatorcontrib><creatorcontrib>Jin, Jianping</creatorcontrib><creatorcontrib>de Stanchina, Elisa</creatorcontrib><creatorcontrib>McCurrach, Mila E.</creatorcontrib><creatorcontrib>Narita, Masashi</creatorcontrib><creatorcontrib>Fuchs, Miriam</creatorcontrib><creatorcontrib>Livingston, David M.</creatorcontrib><creatorcontrib>Lowe, Scott W.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Samuelson, Andrew V.</au><au>Narita, Masako</au><au>Chan, Ho-Man</au><au>Jin, Jianping</au><au>de Stanchina, Elisa</au><au>McCurrach, Mila E.</au><au>Narita, Masashi</au><au>Fuchs, Miriam</au><au>Livingston, David M.</au><au>Lowe, Scott W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>p400 Is Required for E1A to Promote Apoptosis</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>2005-06-10</date><risdate>2005</risdate><volume>280</volume><issue>23</issue><spage>21915</spage><epage>21923</epage><pages>21915-21923</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>The adenovirus E1A oncoprotein promotes proliferation and transformation by binding cellular proteins, including members of the retinoblastoma protein family, the p300/CREB-binding protein transcriptional coactivators, and the p400-TRRAP chromatin-remodeling complex. E1A also promotes apoptosis, in part, by engaging the ARF-p53 tumor suppressor pathway. We show that E1A induces ARF and p53 and promotes apoptosis in normal fibroblasts by physically associating with the retinoblastoma protein and a p400-TRRAP complex and that its interaction with p300 is largely dispensable for these effects. We further show that E1A increases p400 expression and, conversely, that suppression of p400 using stable RNA interference reduces the levels of ARF, p53, and apoptosis in E1A-expressing cells. Therefore, whereas E1A inactivates the retinoblastoma protein, it requires p400 to efficiently promote cell death. These results identify p400 as a regulator of the ARF-p53 pathway and a component of the cellular machinery that couples proliferation to cell death.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>15741165</pmid><doi>10.1074/jbc.M414564200</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenovirus Adenovirus E1A Proteins - metabolism Adenovirus E1A Proteins - physiology ADP-Ribosylation Factors - metabolism Animals Apoptosis Binding Sites Blotting, Northern Blotting, Western Cell Line Cell Survival Chromatin - metabolism DNA Helicases - metabolism DNA Helicases - physiology DNA-Binding Proteins - metabolism DNA-Binding Proteins - physiology Dose-Response Relationship, Drug Doxorubicin - pharmacology E1A-Associated p300 Protein Fibroblasts - metabolism Gene Deletion Gene Expression Regulation Gene Transfer Techniques Genetic Vectors Humans Immunoblotting Immunoprecipitation Mice Microscopy, Fluorescence Mutation Nuclear Proteins - metabolism Protein Binding Protein Structure, Tertiary Retinoblastoma Protein - metabolism Retroviridae - genetics RNA Interference Structure-Activity Relationship Trans-Activators - metabolism Transcriptional Activation Tumor Suppressor Protein p53 - metabolism |
| title | p400 Is Required for E1A to Promote Apoptosis |
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