Physical and functional link of the leukemia-associated factors AML1 and PML
The AML1-CBFβ transcription factor complex is the most frequent target of specific chromosome translocations in acute myeloid leukemia (AML). The promyelocytic leukemia (PML) gene is also frequently involved in AML-associated translocation. Here we report that a specific isoform PML I forms a comple...
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| Veröffentlicht in: | Blood 2005-01, Vol.105 (1), p.292-300 |
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| creator | Nguyen, Lan Anh Pandolfi, Pier Paolo Aikawa, Yukiko Tagata, Yusuke Ohki, Misao Kitabayashi, Issay |
| description | The AML1-CBFβ transcription factor complex is the most frequent target of specific chromosome translocations in acute myeloid leukemia (AML). The promyelocytic leukemia (PML) gene is also frequently involved in AML-associated translocation. Here we report that a specific isoform PML I forms a complex with AML1. PML I was able to recruit AML1 and coactivator p300 in PML nuclear bodies and enhance the AML1-mediated transcription in the presence of p300. A specific C-terminal region of PML I and a C-terminal region of AML1 were found to be required for both their association and colocalization in the nuclear bodies. Overexpression of PML I stimulates myeloid cells to differentiate. These results suggest that PML I could act as a mediator for AML1 and its coactivator p300/CBP to assemble into functional complexes and, consequently, activate AML1-dependent transcription and myeloid cell differentiation. (Blood. 2005;105:292-300) |
| doi_str_mv | 10.1182/blood-2004-03-1185 |
| format | Article |
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The promyelocytic leukemia (PML) gene is also frequently involved in AML-associated translocation. Here we report that a specific isoform PML I forms a complex with AML1. PML I was able to recruit AML1 and coactivator p300 in PML nuclear bodies and enhance the AML1-mediated transcription in the presence of p300. A specific C-terminal region of PML I and a C-terminal region of AML1 were found to be required for both their association and colocalization in the nuclear bodies. Overexpression of PML I stimulates myeloid cells to differentiate. These results suggest that PML I could act as a mediator for AML1 and its coactivator p300/CBP to assemble into functional complexes and, consequently, activate AML1-dependent transcription and myeloid cell differentiation. 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Myelofibrosis ; Medical sciences ; Mice ; Molecular Sequence Data ; Myeloid Cells - cytology ; Myeloid Cells - drug effects ; Neoplasm Proteins - genetics ; Neoplasm Proteins - metabolism ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Promyelocytic Leukemia Protein ; Protein Binding ; Protein Isoforms - chemistry ; Protein Isoforms - genetics ; Protein Isoforms - metabolism ; Protein Structure, Tertiary ; Proto-Oncogene Proteins - chemistry ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins - metabolism ; Sequence Alignment ; Signal Transduction ; Trans-Activators - metabolism ; Transcription Factors - chemistry ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Tumor Suppressor Proteins</subject><ispartof>Blood, 2005-01, Vol.105 (1), p.292-300</ispartof><rights>2005 American Society of Hematology</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c494t-f8be3f6d2d3d0a7660a422761f105184fdcc1408a77ee31a6d0cec124c758a933</citedby><cites>FETCH-LOGICAL-c494t-f8be3f6d2d3d0a7660a422761f105184fdcc1408a77ee31a6d0cec124c758a933</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16423498$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15331439$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nguyen, Lan Anh</creatorcontrib><creatorcontrib>Pandolfi, Pier Paolo</creatorcontrib><creatorcontrib>Aikawa, Yukiko</creatorcontrib><creatorcontrib>Tagata, Yusuke</creatorcontrib><creatorcontrib>Ohki, Misao</creatorcontrib><creatorcontrib>Kitabayashi, Issay</creatorcontrib><title>Physical and functional link of the leukemia-associated factors AML1 and PML</title><title>Blood</title><addtitle>Blood</addtitle><description>The AML1-CBFβ transcription factor complex is the most frequent target of specific chromosome translocations in acute myeloid leukemia (AML). The promyelocytic leukemia (PML) gene is also frequently involved in AML-associated translocation. Here we report that a specific isoform PML I forms a complex with AML1. PML I was able to recruit AML1 and coactivator p300 in PML nuclear bodies and enhance the AML1-mediated transcription in the presence of p300. A specific C-terminal region of PML I and a C-terminal region of AML1 were found to be required for both their association and colocalization in the nuclear bodies. Overexpression of PML I stimulates myeloid cells to differentiate. These results suggest that PML I could act as a mediator for AML1 and its coactivator p300/CBP to assemble into functional complexes and, consequently, activate AML1-dependent transcription and myeloid cell differentiation. (Blood. 2005;105:292-300)</description><subject>Active Transport, Cell Nucleus</subject><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Binding Sites</subject><subject>Biological and medical sciences</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Line, Tumor</subject><subject>Cell Nucleus - metabolism</subject><subject>Core Binding Factor Alpha 2 Subunit</subject><subject>DNA-Binding Proteins - chemistry</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>E1A-Associated p300 Protein</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Granulocyte Colony-Stimulating Factor - pharmacology</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Leukemia - metabolism</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Molecular Sequence Data</subject><subject>Myeloid Cells - cytology</subject><subject>Myeloid Cells - drug effects</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Promyelocytic Leukemia Protein</subject><subject>Protein Binding</subject><subject>Protein Isoforms - chemistry</subject><subject>Protein Isoforms - genetics</subject><subject>Protein Isoforms - metabolism</subject><subject>Protein Structure, Tertiary</subject><subject>Proto-Oncogene Proteins - chemistry</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Sequence Alignment</subject><subject>Signal Transduction</subject><subject>Trans-Activators - metabolism</subject><subject>Transcription Factors - chemistry</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Tumor Suppressor Proteins</subject><issn>0006-4971</issn><issn>1528-0020</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMlKBDEQhoMoOi4v4EH6ordoZekNvMjgBi160HPIJBWM9nQ06RZ8ezPOgDdPtfD9RfERcszgnLGGXyz6ECzlAJKCoHlVbpEZK3lDAThskxkAVFS2Ndsj-ym9ATApeLlL9lgpRO7bGemeXr-TN7ov9GALNw1m9GHIY--H9yK4YnzFosfpHZdeU51SMF6PmFFtxhBTcfXQsd_s00N3SHac7hMebeoBebm5fp7f0e7x9n5-1VEjWzlS1yxQuMpyKyzouqpAS87rijkGJWuks8YwCY2ua0TBdGXBoGFcmrpsdCvEATlb3_2I4XPCNKqlTwb7Xg8YpqSqWvBaNG0G-Ro0MaQU0amP6Jc6fisGauVQ_TpUK4cKxGpV5tDJ5vq0WKL9i2ykZeB0A-iUzbmoB-PTH1dJLmTbZO5yzWF28eUxqmQ8Dgatj2hGZYP_748f0xyN6A</recordid><startdate>20050101</startdate><enddate>20050101</enddate><creator>Nguyen, Lan Anh</creator><creator>Pandolfi, Pier Paolo</creator><creator>Aikawa, Yukiko</creator><creator>Tagata, Yusuke</creator><creator>Ohki, Misao</creator><creator>Kitabayashi, Issay</creator><general>Elsevier Inc</general><general>The Americain Society of Hematology</general><scope>6I.</scope><scope>AAFTH</scope><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>7X8</scope></search><sort><creationdate>20050101</creationdate><title>Physical and functional link of the leukemia-associated factors AML1 and PML</title><author>Nguyen, Lan Anh ; Pandolfi, Pier Paolo ; Aikawa, Yukiko ; Tagata, Yusuke ; Ohki, Misao ; Kitabayashi, Issay</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c494t-f8be3f6d2d3d0a7660a422761f105184fdcc1408a77ee31a6d0cec124c758a933</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Active Transport, Cell Nucleus</topic><topic>Amino Acid Sequence</topic><topic>Animals</topic><topic>Binding Sites</topic><topic>Biological and medical sciences</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Line, Tumor</topic><topic>Cell Nucleus - metabolism</topic><topic>Core Binding Factor Alpha 2 Subunit</topic><topic>DNA-Binding Proteins - chemistry</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>E1A-Associated p300 Protein</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Granulocyte Colony-Stimulating Factor - pharmacology</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Leukemia - metabolism</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Molecular Sequence Data</topic><topic>Myeloid Cells - cytology</topic><topic>Myeloid Cells - drug effects</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Promyelocytic Leukemia Protein</topic><topic>Protein Binding</topic><topic>Protein Isoforms - chemistry</topic><topic>Protein Isoforms - genetics</topic><topic>Protein Isoforms - metabolism</topic><topic>Protein Structure, Tertiary</topic><topic>Proto-Oncogene Proteins - chemistry</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Sequence Alignment</topic><topic>Signal Transduction</topic><topic>Trans-Activators - metabolism</topic><topic>Transcription Factors - chemistry</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Tumor Suppressor Proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nguyen, Lan Anh</creatorcontrib><creatorcontrib>Pandolfi, Pier Paolo</creatorcontrib><creatorcontrib>Aikawa, Yukiko</creatorcontrib><creatorcontrib>Tagata, Yusuke</creatorcontrib><creatorcontrib>Ohki, Misao</creatorcontrib><creatorcontrib>Kitabayashi, Issay</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>MEDLINE - Academic</collection><jtitle>Blood</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nguyen, Lan Anh</au><au>Pandolfi, Pier Paolo</au><au>Aikawa, Yukiko</au><au>Tagata, Yusuke</au><au>Ohki, Misao</au><au>Kitabayashi, Issay</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Physical and functional link of the leukemia-associated factors AML1 and PML</atitle><jtitle>Blood</jtitle><addtitle>Blood</addtitle><date>2005-01-01</date><risdate>2005</risdate><volume>105</volume><issue>1</issue><spage>292</spage><epage>300</epage><pages>292-300</pages><issn>0006-4971</issn><eissn>1528-0020</eissn><abstract>The AML1-CBFβ transcription factor complex is the most frequent target of specific chromosome translocations in acute myeloid leukemia (AML). The promyelocytic leukemia (PML) gene is also frequently involved in AML-associated translocation. Here we report that a specific isoform PML I forms a complex with AML1. PML I was able to recruit AML1 and coactivator p300 in PML nuclear bodies and enhance the AML1-mediated transcription in the presence of p300. A specific C-terminal region of PML I and a C-terminal region of AML1 were found to be required for both their association and colocalization in the nuclear bodies. Overexpression of PML I stimulates myeloid cells to differentiate. These results suggest that PML I could act as a mediator for AML1 and its coactivator p300/CBP to assemble into functional complexes and, consequently, activate AML1-dependent transcription and myeloid cell differentiation. (Blood. 2005;105:292-300)</abstract><cop>Washington, DC</cop><pub>Elsevier Inc</pub><pmid>15331439</pmid><doi>10.1182/blood-2004-03-1185</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Active Transport, Cell Nucleus Amino Acid Sequence Animals Binding Sites Biological and medical sciences Cell Differentiation - drug effects Cell Line, Tumor Cell Nucleus - metabolism Core Binding Factor Alpha 2 Subunit DNA-Binding Proteins - chemistry DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism E1A-Associated p300 Protein Gene Expression Regulation, Neoplastic Granulocyte Colony-Stimulating Factor - pharmacology Hematologic and hematopoietic diseases Humans Leukemia - metabolism Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Medical sciences Mice Molecular Sequence Data Myeloid Cells - cytology Myeloid Cells - drug effects Neoplasm Proteins - genetics Neoplasm Proteins - metabolism Nuclear Proteins - genetics Nuclear Proteins - metabolism Promyelocytic Leukemia Protein Protein Binding Protein Isoforms - chemistry Protein Isoforms - genetics Protein Isoforms - metabolism Protein Structure, Tertiary Proto-Oncogene Proteins - chemistry Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Sequence Alignment Signal Transduction Trans-Activators - metabolism Transcription Factors - chemistry Transcription Factors - genetics Transcription Factors - metabolism Tumor Suppressor Proteins |
| title | Physical and functional link of the leukemia-associated factors AML1 and PML |
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