PU.1 binding to the p53 family of tumor suppressors impairs their transcriptional activity
The transcription factor PU.1 is essential for terminal myeloid differentiation, B- and T-cell development, erythropoiesis and hematopoietic stem cell maintenance. PU.1 functions as oncogene in Friend virus-induced erythroleukemia and as tumor suppressor in acute myeloid leukemias. Moreover, Friend...
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| Veröffentlicht in: | Oncogene 2008-05, Vol.27 (24), p.3489-3493 |
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| creator | Tschan, M P Reddy, V A Ress, A Arvidsson, G Fey, M F Torbett, B E |
| description | The transcription factor PU.1 is essential for terminal myeloid differentiation, B- and T-cell development, erythropoiesis and hematopoietic stem cell maintenance. PU.1 functions as oncogene in Friend virus-induced erythroleukemia and as tumor suppressor in acute myeloid leukemias. Moreover, Friend virus-induced erythroleukemia requires maintenance of PU.1 expression and the disruption of p53 function greatly accelerates disease progression. It has been hypothesized that p53-mediated expression of the p21
Cip1
cell cycle inhibitor during differentiation of pre-erythroleukemia cells promotes selection against p53 function. In addition to the blockage of erythroblast differentiation provided by increased levels of PU.1, we propose that PU.1 alters p53 function. We demonstrate that PU.1 reduces the transcriptional activity of the p53 tumor suppressor family and thus inhibits activation of genes important for cell cycle regulation and apoptosis. Inhibition is mediated through binding of PU.1 to the DNA-binding and/or oligomerization domains of p53/p73 proteins. Lastly, knocking down endogenous PU.1 in p53 wild-type REH B-cell precursor leukemia cells leads to increased expression of the p53 target p21
Cip1
. |
| doi_str_mv | 10.1038/sj.onc.1211004 |
| format | Article |
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Cip1
cell cycle inhibitor during differentiation of pre-erythroleukemia cells promotes selection against p53 function. In addition to the blockage of erythroblast differentiation provided by increased levels of PU.1, we propose that PU.1 alters p53 function. We demonstrate that PU.1 reduces the transcriptional activity of the p53 tumor suppressor family and thus inhibits activation of genes important for cell cycle regulation and apoptosis. Inhibition is mediated through binding of PU.1 to the DNA-binding and/or oligomerization domains of p53/p73 proteins. Lastly, knocking down endogenous PU.1 in p53 wild-type REH B-cell precursor leukemia cells leads to increased expression of the p53 target p21
Cip1
.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1211004</identifier><identifier>PMID: 18193090</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Acute leukemia ; Apoptosis ; Binding sites ; Biological and medical sciences ; Blotting, Western ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cell Biology ; Cell cycle ; Cell differentiation ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Cyclin-dependent kinase inhibitor p21 ; Cyclin-Dependent Kinase Inhibitor p21 - genetics ; Cyclin-Dependent Kinase Inhibitor p21 - metabolism ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Erythroleukemia ; Erythropoiesis ; Fundamental and applied biological sciences. Psychology ; Genetic aspects ; Genetic transcription ; Genetics ; Hematopoietic stem cells ; Human Genetics ; Humans ; Immunoprecipitation ; Internal Medicine ; Leukemia ; Lymphocytes B ; Lymphocytes T ; Medicine ; Medicine & Public Health ; Molecular and cellular biology ; Molecular genetics ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Oligomerization ; Oncology ; p53 Protein ; Physiological aspects ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - metabolism ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - pathology ; Protein Isoforms ; Proto-Oncogene Proteins - antagonists & inhibitors ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins - metabolism ; PU.1 protein ; Risk factors ; RNA, Small Interfering - pharmacology ; short-communication ; Stem cells ; Trans-Activators - antagonists & inhibitors ; Trans-Activators - genetics ; Trans-Activators - metabolism ; Transcription activation ; Transcription, Genetic ; Transcription. Transcription factor. Splicing. Rna processing ; Transcriptional Activation ; Tumor Cells, Cultured ; Tumor Protein p73 ; Tumor suppressor genes ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism ; Tumor Suppressor Proteins - genetics ; Tumor Suppressor Proteins - metabolism ; Tumors ; Viruses</subject><ispartof>Oncogene, 2008-05, Vol.27 (24), p.3489-3493</ispartof><rights>Springer Nature Limited 2008</rights><rights>2008 INIST-CNRS</rights><rights>COPYRIGHT 2008 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group May 29, 2008</rights><rights>Nature Publishing Group 2008.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c569t-28dad9c962a170938a47bbc9f5ca54fbe3e6bfbb4a455800eea331451c46dd3d3</citedby><cites>FETCH-LOGICAL-c569t-28dad9c962a170938a47bbc9f5ca54fbe3e6bfbb4a455800eea331451c46dd3d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.onc.1211004$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.onc.1211004$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,2727,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20443740$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18193090$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tschan, M P</creatorcontrib><creatorcontrib>Reddy, V A</creatorcontrib><creatorcontrib>Ress, A</creatorcontrib><creatorcontrib>Arvidsson, G</creatorcontrib><creatorcontrib>Fey, M F</creatorcontrib><creatorcontrib>Torbett, B E</creatorcontrib><title>PU.1 binding to the p53 family of tumor suppressors impairs their transcriptional activity</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>The transcription factor PU.1 is essential for terminal myeloid differentiation, B- and T-cell development, erythropoiesis and hematopoietic stem cell maintenance. PU.1 functions as oncogene in Friend virus-induced erythroleukemia and as tumor suppressor in acute myeloid leukemias. Moreover, Friend virus-induced erythroleukemia requires maintenance of PU.1 expression and the disruption of p53 function greatly accelerates disease progression. It has been hypothesized that p53-mediated expression of the p21
Cip1
cell cycle inhibitor during differentiation of pre-erythroleukemia cells promotes selection against p53 function. In addition to the blockage of erythroblast differentiation provided by increased levels of PU.1, we propose that PU.1 alters p53 function. We demonstrate that PU.1 reduces the transcriptional activity of the p53 tumor suppressor family and thus inhibits activation of genes important for cell cycle regulation and apoptosis. Inhibition is mediated through binding of PU.1 to the DNA-binding and/or oligomerization domains of p53/p73 proteins. Lastly, knocking down endogenous PU.1 in p53 wild-type REH B-cell precursor leukemia cells leads to increased expression of the p53 target p21
Cip1
.</description><subject>Acute leukemia</subject><subject>Apoptosis</subject><subject>Binding sites</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell Biology</subject><subject>Cell cycle</subject><subject>Cell differentiation</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Cyclin-dependent kinase inhibitor p21</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - genetics</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Erythroleukemia</subject><subject>Erythropoiesis</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genetic aspects</subject><subject>Genetic transcription</subject><subject>Genetics</subject><subject>Hematopoietic stem cells</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Internal Medicine</subject><subject>Leukemia</subject><subject>Lymphocytes B</subject><subject>Lymphocytes T</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Oligomerization</subject><subject>Oncology</subject><subject>p53 Protein</subject><subject>Physiological aspects</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma - metabolism</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma - pathology</subject><subject>Protein Isoforms</subject><subject>Proto-Oncogene Proteins - antagonists & inhibitors</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>PU.1 protein</subject><subject>Risk factors</subject><subject>RNA, Small Interfering - pharmacology</subject><subject>short-communication</subject><subject>Stem cells</subject><subject>Trans-Activators - antagonists & inhibitors</subject><subject>Trans-Activators - genetics</subject><subject>Trans-Activators - metabolism</subject><subject>Transcription activation</subject><subject>Transcription, Genetic</subject><subject>Transcription. Transcription factor. Splicing. Rna processing</subject><subject>Transcriptional Activation</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Protein p73</subject><subject>Tumor suppressor genes</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Tumor Suppressor Proteins - genetics</subject><subject>Tumor Suppressor Proteins - metabolism</subject><subject>Tumors</subject><subject>Viruses</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</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>eNqFks9rFDEUx4Modlu9elOCoreZ5udkcizFqlDQg714CZlMZs0yk4xJprD_vVl2cEFaSgiBvM_7vryXLwBvMKoxou1l2tXBmxoTjBFiz8AGM9FUnEv2HGyQ5KiShJIzcJ7SDiEkJCIvwRlusaRIog349eOuxrBzvnd-C3OA-beFM6dw0JMb9zAMMC9TiDAt8xxtSiEm6KZZu3IW1kWYo_bJRDdnF7weoTbZ3bu8fwVeDHpM9vV6XoC7m88_r79Wt9-_fLu-uq0Mb2SuSNvrXhrZEI0FkrTVTHSdkQM3mrOhs9Q23dB1TDPOW4Ss1ZRixrFhTd_Tnl6AT0fdOYY_i01ZTS4ZO47a27AkJZBoGcPNkyDBRbjsJ0EsBccC8wJ--A_chSWWIRSxhmHa8laQQr1_lCKCspYKdpLa6tEq54dQ5moOddUVlkgwKdqDVP0AVVZvJ2eCt4Mr9w8lmBhSinZQc3STjnuFkTo4SKWdKg5Sq4NKwrv1sUs32f6Er5YpwMcV0MnocSi_b1z6xxHEWOnnwF0euVRCfmvjqetHS789Znidl2hPpdf4X1ta5ZI</recordid><startdate>20080529</startdate><enddate>20080529</enddate><creator>Tschan, M P</creator><creator>Reddy, V A</creator><creator>Ress, A</creator><creator>Arvidsson, G</creator><creator>Fey, M F</creator><creator>Torbett, B E</creator><general>Nature Publishing Group UK</general><general>Nature Publishing</general><general>Nature Publishing Group</general><scope>IQODW</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>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>Q9U</scope><scope>RC3</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20080529</creationdate><title>PU.1 binding to the p53 family of tumor suppressors impairs their transcriptional activity</title><author>Tschan, M P ; Reddy, V A ; Ress, A ; Arvidsson, G ; Fey, M F ; Torbett, B E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c569t-28dad9c962a170938a47bbc9f5ca54fbe3e6bfbb4a455800eea331451c46dd3d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Acute leukemia</topic><topic>Apoptosis</topic><topic>Binding sites</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cell Biology</topic><topic>Cell cycle</topic><topic>Cell differentiation</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Cyclin-dependent kinase inhibitor p21</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - genetics</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Erythroleukemia</topic><topic>Erythropoiesis</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genetic aspects</topic><topic>Genetic transcription</topic><topic>Genetics</topic><topic>Hematopoietic stem cells</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Immunoprecipitation</topic><topic>Internal Medicine</topic><topic>Leukemia</topic><topic>Lymphocytes B</topic><topic>Lymphocytes T</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Oligomerization</topic><topic>Oncology</topic><topic>p53 Protein</topic><topic>Physiological aspects</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma - metabolism</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma - pathology</topic><topic>Protein Isoforms</topic><topic>Proto-Oncogene Proteins - antagonists & inhibitors</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>PU.1 protein</topic><topic>Risk factors</topic><topic>RNA, Small Interfering - pharmacology</topic><topic>short-communication</topic><topic>Stem cells</topic><topic>Trans-Activators - antagonists & inhibitors</topic><topic>Trans-Activators - genetics</topic><topic>Trans-Activators - metabolism</topic><topic>Transcription activation</topic><topic>Transcription, Genetic</topic><topic>Transcription. Transcription factor. Splicing. Rna processing</topic><topic>Transcriptional Activation</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Protein p73</topic><topic>Tumor suppressor genes</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Tumor Suppressor Proteins - genetics</topic><topic>Tumor Suppressor Proteins - metabolism</topic><topic>Tumors</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tschan, M P</creatorcontrib><creatorcontrib>Reddy, V A</creatorcontrib><creatorcontrib>Ress, A</creatorcontrib><creatorcontrib>Arvidsson, G</creatorcontrib><creatorcontrib>Fey, M F</creatorcontrib><creatorcontrib>Torbett, B E</creatorcontrib><collection>Pascal-Francis</collection><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>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 Basic</collection><collection>Genetics Abstracts</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tschan, M P</au><au>Reddy, V A</au><au>Ress, A</au><au>Arvidsson, G</au><au>Fey, M F</au><au>Torbett, B E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PU.1 binding to the p53 family of tumor suppressors impairs their transcriptional activity</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2008-05-29</date><risdate>2008</risdate><volume>27</volume><issue>24</issue><spage>3489</spage><epage>3493</epage><pages>3489-3493</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>The transcription factor PU.1 is essential for terminal myeloid differentiation, B- and T-cell development, erythropoiesis and hematopoietic stem cell maintenance. PU.1 functions as oncogene in Friend virus-induced erythroleukemia and as tumor suppressor in acute myeloid leukemias. Moreover, Friend virus-induced erythroleukemia requires maintenance of PU.1 expression and the disruption of p53 function greatly accelerates disease progression. It has been hypothesized that p53-mediated expression of the p21
Cip1
cell cycle inhibitor during differentiation of pre-erythroleukemia cells promotes selection against p53 function. In addition to the blockage of erythroblast differentiation provided by increased levels of PU.1, we propose that PU.1 alters p53 function. We demonstrate that PU.1 reduces the transcriptional activity of the p53 tumor suppressor family and thus inhibits activation of genes important for cell cycle regulation and apoptosis. Inhibition is mediated through binding of PU.1 to the DNA-binding and/or oligomerization domains of p53/p73 proteins. Lastly, knocking down endogenous PU.1 in p53 wild-type REH B-cell precursor leukemia cells leads to increased expression of the p53 target p21
Cip1
.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>18193090</pmid><doi>10.1038/sj.onc.1211004</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0950-9232 |
| ispartof | Oncogene, 2008-05, Vol.27 (24), p.3489-3493 |
| issn | 0950-9232 1476-5594 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_70784416 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Nature Journals Online; SpringerLink Journals - AutoHoldings |
| subjects | Acute leukemia Apoptosis Binding sites Biological and medical sciences Blotting, Western Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cell Biology Cell cycle Cell differentiation Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cyclin-dependent kinase inhibitor p21 Cyclin-Dependent Kinase Inhibitor p21 - genetics Cyclin-Dependent Kinase Inhibitor p21 - metabolism DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Erythroleukemia Erythropoiesis Fundamental and applied biological sciences. Psychology Genetic aspects Genetic transcription Genetics Hematopoietic stem cells Human Genetics Humans Immunoprecipitation Internal Medicine Leukemia Lymphocytes B Lymphocytes T Medicine Medicine & Public Health Molecular and cellular biology Molecular genetics Nuclear Proteins - genetics Nuclear Proteins - metabolism Oligomerization Oncology p53 Protein Physiological aspects Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics Precursor Cell Lymphoblastic Leukemia-Lymphoma - metabolism Precursor Cell Lymphoblastic Leukemia-Lymphoma - pathology Protein Isoforms Proto-Oncogene Proteins - antagonists & inhibitors Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism PU.1 protein Risk factors RNA, Small Interfering - pharmacology short-communication Stem cells Trans-Activators - antagonists & inhibitors Trans-Activators - genetics Trans-Activators - metabolism Transcription activation Transcription, Genetic Transcription. Transcription factor. Splicing. Rna processing Transcriptional Activation Tumor Cells, Cultured Tumor Protein p73 Tumor suppressor genes Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - metabolism Tumors Viruses |
| title | PU.1 binding to the p53 family of tumor suppressors impairs their transcriptional activity |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T13%3A01%3A12IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=PU.1%20binding%20to%20the%20p53%20family%20of%20tumor%20suppressors%20impairs%20their%20transcriptional%20activity&rft.jtitle=Oncogene&rft.au=Tschan,%20M%20P&rft.date=2008-05-29&rft.volume=27&rft.issue=24&rft.spage=3489&rft.epage=3493&rft.pages=3489-3493&rft.issn=0950-9232&rft.eissn=1476-5594&rft.coden=ONCNES&rft_id=info:doi/10.1038/sj.onc.1211004&rft_dat=%3Cgale_proqu%3EA190749782%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=227348374&rft_id=info:pmid/18193090&rft_galeid=A190749782&rfr_iscdi=true |