Deregulated expression of E2F1 promotes proteolytic degradation of tumor suppressor p73 and inhibits its transcriptional activity
The expression of tumor suppressor p73 is regulated at mRNA and protein levels. It has been shown that E2F1 acts as a transcriptional activator for p73. In this study, we have found that deregulated expression of E2F1 increases the mRNA level of p73, however, E2F1 promotes the degradation of p73. Im...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2009-09, Vol.387 (1), p.143-148 |
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| container_title | Biochemical and biophysical research communications |
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| creator | Ozaki, Toshinori Okoshi, Rintaro Ono, Sayaka Kubo, Natsumi Nakagawara, Akira |
| description | The expression of tumor suppressor p73 is regulated at mRNA and protein levels. It has been shown that E2F1 acts as a transcriptional activator for
p73. In this study, we have found that deregulated expression of E2F1 increases the mRNA level of
p73, however, E2F1 promotes the degradation of p73. Immunoprecipitation experiments demonstrated that E2F1 forms a complex with p73 and inhibits the transcriptional activity of p73. Enforced expression of E2F1 induces degradation of p73 in a proteasome-independent manner. Additionally, the deletion analysis showed that E2F1(1–117) has an undetectable effect on p73, whereas E2F1(1–285) and E2F1(1–414) have an ability to promote degradation of p73 and inhibition of p73 transcriptional activity, suggesting that the region of E2F1 between amino acid residues 118 and 285 has a critical role in the regulation of p73. Taken together, our present study indicates that E2F1 has a dual role in the regulation of p73. |
| doi_str_mv | 10.1016/j.bbrc.2009.06.141 |
| format | Article |
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p73. In this study, we have found that deregulated expression of E2F1 increases the mRNA level of
p73, however, E2F1 promotes the degradation of p73. Immunoprecipitation experiments demonstrated that E2F1 forms a complex with p73 and inhibits the transcriptional activity of p73. Enforced expression of E2F1 induces degradation of p73 in a proteasome-independent manner. Additionally, the deletion analysis showed that E2F1(1–117) has an undetectable effect on p73, whereas E2F1(1–285) and E2F1(1–414) have an ability to promote degradation of p73 and inhibition of p73 transcriptional activity, suggesting that the region of E2F1 between amino acid residues 118 and 285 has a critical role in the regulation of p73. Taken together, our present study indicates that E2F1 has a dual role in the regulation of p73.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2009.06.141</identifier><identifier>PMID: 19576172</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Cell Line, Tumor ; DNA Mutational Analysis ; DNA-Binding Proteins - antagonists & inhibitors ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; E2F1 ; E2F1 Transcription Factor - genetics ; E2F1 Transcription Factor - metabolism ; Humans ; Immunoprecipitation ; MG-132 ; Nuclear Proteins - antagonists & inhibitors ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; p73 ; Proteasome ; Proteasome Endopeptidase Complex - metabolism ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Sequence Deletion ; Trans-Activators ; Transcription, Genetic ; Tumor Protein p73 ; Tumor Suppressor Proteins - antagonists & inhibitors ; Tumor Suppressor Proteins - genetics ; Tumor Suppressor Proteins - metabolism</subject><ispartof>Biochemical and biophysical research communications, 2009-09, Vol.387 (1), p.143-148</ispartof><rights>2009 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-2c7299c7152180e608bb7bf67989d90c7edb7ffcc1929807afb249854b132d093</citedby><cites>FETCH-LOGICAL-c451t-2c7299c7152180e608bb7bf67989d90c7edb7ffcc1929807afb249854b132d093</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbrc.2009.06.141$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19576172$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ozaki, Toshinori</creatorcontrib><creatorcontrib>Okoshi, Rintaro</creatorcontrib><creatorcontrib>Ono, Sayaka</creatorcontrib><creatorcontrib>Kubo, Natsumi</creatorcontrib><creatorcontrib>Nakagawara, Akira</creatorcontrib><title>Deregulated expression of E2F1 promotes proteolytic degradation of tumor suppressor p73 and inhibits its transcriptional activity</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>The expression of tumor suppressor p73 is regulated at mRNA and protein levels. It has been shown that E2F1 acts as a transcriptional activator for
p73. In this study, we have found that deregulated expression of E2F1 increases the mRNA level of
p73, however, E2F1 promotes the degradation of p73. Immunoprecipitation experiments demonstrated that E2F1 forms a complex with p73 and inhibits the transcriptional activity of p73. Enforced expression of E2F1 induces degradation of p73 in a proteasome-independent manner. Additionally, the deletion analysis showed that E2F1(1–117) has an undetectable effect on p73, whereas E2F1(1–285) and E2F1(1–414) have an ability to promote degradation of p73 and inhibition of p73 transcriptional activity, suggesting that the region of E2F1 between amino acid residues 118 and 285 has a critical role in the regulation of p73. Taken together, our present study indicates that E2F1 has a dual role in the regulation of p73.</description><subject>Cell Line, Tumor</subject><subject>DNA Mutational Analysis</subject><subject>DNA-Binding Proteins - antagonists & inhibitors</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>E2F1</subject><subject>E2F1 Transcription Factor - genetics</subject><subject>E2F1 Transcription Factor - metabolism</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>MG-132</subject><subject>Nuclear Proteins - antagonists & inhibitors</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>p73</subject><subject>Proteasome</subject><subject>Proteasome Endopeptidase Complex - metabolism</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Sequence Deletion</subject><subject>Trans-Activators</subject><subject>Transcription, Genetic</subject><subject>Tumor Protein p73</subject><subject>Tumor Suppressor Proteins - antagonists & inhibitors</subject><subject>Tumor Suppressor Proteins - genetics</subject><subject>Tumor Suppressor Proteins - metabolism</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU2LFDEQhoMo7uzqH_AgOXnrtir9kQl4kXV3FRa8KHgL-aheM_SXSXpxjv5zu50Bb3oIVYfnfSH1MPYKoUTA9u2htDa6UgCoEtoSa3zCdggKCoFQP2U7AGgLofDbBbtM6QCAWLfqObtA1cgWpdixXx8o0sPSm0ye0885UkphGvnU8Rtxi3yO0zBlStuSaeqPOTju6SEab_IZzMswRZ6W-U96XWdZcTN6HsbvwYac-PZyNGNyMcxbzPTcuBweQz6-YM860yd6eZ5X7OvtzZfrj8X957tP1-_vC1c3mAvhpFDKSWwE7oFa2FsrbddKtVdegZPkrew651AJtQdpOitqtW9qi5XwoKor9ubUu_7kx0Ip6yEkR31vRpqWpFvZVEpU8F9QrLdXQlQrKE6gi1NKkTo9xzCYeNQIejOkD3ozpDdDGlq9GlpDr8_tix3I_42clazAuxNA6zEeA0WdXKDRkQ-RXNZ-Cv_q_w1buaRF</recordid><startdate>20090911</startdate><enddate>20090911</enddate><creator>Ozaki, Toshinori</creator><creator>Okoshi, Rintaro</creator><creator>Ono, Sayaka</creator><creator>Kubo, Natsumi</creator><creator>Nakagawara, Akira</creator><general>Elsevier Inc</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>7TM</scope><scope>7TO</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20090911</creationdate><title>Deregulated expression of E2F1 promotes proteolytic degradation of tumor suppressor p73 and inhibits its transcriptional activity</title><author>Ozaki, Toshinori ; Okoshi, Rintaro ; Ono, Sayaka ; Kubo, Natsumi ; Nakagawara, Akira</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c451t-2c7299c7152180e608bb7bf67989d90c7edb7ffcc1929807afb249854b132d093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Cell Line, Tumor</topic><topic>DNA Mutational Analysis</topic><topic>DNA-Binding Proteins - antagonists & inhibitors</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>E2F1</topic><topic>E2F1 Transcription Factor - genetics</topic><topic>E2F1 Transcription Factor - metabolism</topic><topic>Humans</topic><topic>Immunoprecipitation</topic><topic>MG-132</topic><topic>Nuclear Proteins - antagonists & inhibitors</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>p73</topic><topic>Proteasome</topic><topic>Proteasome Endopeptidase Complex - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Sequence Deletion</topic><topic>Trans-Activators</topic><topic>Transcription, Genetic</topic><topic>Tumor Protein p73</topic><topic>Tumor Suppressor Proteins - antagonists & inhibitors</topic><topic>Tumor Suppressor Proteins - genetics</topic><topic>Tumor Suppressor Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ozaki, Toshinori</creatorcontrib><creatorcontrib>Okoshi, Rintaro</creatorcontrib><creatorcontrib>Ono, Sayaka</creatorcontrib><creatorcontrib>Kubo, Natsumi</creatorcontrib><creatorcontrib>Nakagawara, Akira</creatorcontrib><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><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ozaki, Toshinori</au><au>Okoshi, Rintaro</au><au>Ono, Sayaka</au><au>Kubo, Natsumi</au><au>Nakagawara, Akira</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Deregulated expression of E2F1 promotes proteolytic degradation of tumor suppressor p73 and inhibits its transcriptional activity</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2009-09-11</date><risdate>2009</risdate><volume>387</volume><issue>1</issue><spage>143</spage><epage>148</epage><pages>143-148</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>The expression of tumor suppressor p73 is regulated at mRNA and protein levels. It has been shown that E2F1 acts as a transcriptional activator for
p73. In this study, we have found that deregulated expression of E2F1 increases the mRNA level of
p73, however, E2F1 promotes the degradation of p73. Immunoprecipitation experiments demonstrated that E2F1 forms a complex with p73 and inhibits the transcriptional activity of p73. Enforced expression of E2F1 induces degradation of p73 in a proteasome-independent manner. Additionally, the deletion analysis showed that E2F1(1–117) has an undetectable effect on p73, whereas E2F1(1–285) and E2F1(1–414) have an ability to promote degradation of p73 and inhibition of p73 transcriptional activity, suggesting that the region of E2F1 between amino acid residues 118 and 285 has a critical role in the regulation of p73. Taken together, our present study indicates that E2F1 has a dual role in the regulation of p73.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>19576172</pmid><doi>10.1016/j.bbrc.2009.06.141</doi><tpages>6</tpages></addata></record> |
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| subjects | Cell Line, Tumor DNA Mutational Analysis DNA-Binding Proteins - antagonists & inhibitors DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism E2F1 E2F1 Transcription Factor - genetics E2F1 Transcription Factor - metabolism Humans Immunoprecipitation MG-132 Nuclear Proteins - antagonists & inhibitors Nuclear Proteins - genetics Nuclear Proteins - metabolism p73 Proteasome Proteasome Endopeptidase Complex - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism Sequence Deletion Trans-Activators Transcription, Genetic Tumor Protein p73 Tumor Suppressor Proteins - antagonists & inhibitors Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - metabolism |
| title | Deregulated expression of E2F1 promotes proteolytic degradation of tumor suppressor p73 and inhibits its transcriptional activity |
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