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PRAM-1 Is a Novel Adaptor Protein Regulated by Retinoic Acid (RA) and Promyelocytic Leukemia (PML)-RA Receptor α in Acute Promyelocytic Leukemia Cells
The t(15;17) translocation, found in 95% of acute promyelocytic leukemia, encodes a promyelocytic leukemia (PML)-retinoic acid receptor α (RARα) fusion protein. Complete remission of acute promyelocytic leukemia can be obtained by treating patients with all-trans retinoic acid, and PML-RARα plays a...
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| Published in: | The Journal of biological chemistry 2001-06, Vol.276 (25), p.22375-22381 |
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| creator | Moog-Lutz, Christel Peterson, Erik J. Lutz, Pierre G. Eliason, Steve Cavé-Riant, Florence Singer, Andrew Di Gioia, Yolande Dmowski, Sally Kamens, Joanne Cayre, Yvon E. Koretzky, Gary |
| description | The t(15;17) translocation, found in 95% of acute promyelocytic leukemia, encodes a promyelocytic leukemia (PML)-retinoic acid receptor α (RARα) fusion protein. Complete remission of acute promyelocytic leukemia can be obtained by treating patients with all-trans retinoic acid, and PML-RARα plays a major role in mediating retinoic acid effects in leukemia cells. A main model proposed for acute promyelocytic leukemia is that PML-RARα exerts its oncogenic effects by repressing the expression of retinoic acid-inducible genes critical to myeloid differentiation. By applying subtraction cloning to acute promyelocytic leukemia cells, we identified a retinoic acid-induced gene, PRAM-1 (PML-RARα target gene encoding anAdaptor Molecule-1), which encodes a novel adaptor protein sharing structural homologies with the SLAP-130/fyb adaptor. PRAM-1 is expressed and regulated during normal human myelopoiesis. In U937 myeloid precursor cells, PRAM-1 expression is inhibited by expression of PML-RARα in the absence of ligand andde novo superinduced by retinoic acid. PRAM-1 associates with other adaptors, SLP-76 and SKAP-55HOM, in myeloid cell lines and with protein tyrosine kinase lyn. By providing the first evidence that PML-RARα dysregulates expression of an adaptor protein, our data open new insights into signaling events that are disrupted during transformation by PML-RARα and induced by retinoic acid duringde novo differentiation of acute promyelocytic leukemia cells.
AJ272324 |
| doi_str_mv | 10.1074/jbc.M011683200 |
| format | article |
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AJ272324</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M011683200</identifier><identifier>PMID: 11301322</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>adaptor protein ; Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Base Sequence ; Cell Differentiation ; chromosome 15 ; chromosome 17 ; Cloning, Molecular ; DNA, Complementary ; Gene Expression Regulation, Neoplastic - drug effects ; Humans ; Leukemia, Promyelocytic, Acute - metabolism ; Leukemia, Promyelocytic, Acute - pathology ; Life Sciences ; Molecular Sequence Data ; Neoplasm Proteins - physiology ; Oncogene Proteins, Fusion - physiology ; PML-RAR^a protein ; PRAM-1 gene ; PRAM-1 protein ; Proteins - chemistry ; Proteins - genetics ; Proteins - metabolism ; retinoic acid receptor ^a ; RNA, Messenger - genetics ; Tretinoin - pharmacology ; Tumor Cells, Cultured ; U937 Cells</subject><ispartof>The Journal of biological chemistry, 2001-06, Vol.276 (25), p.22375-22381</ispartof><rights>2001 © 2001 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c445t-5228564f45d864f1974d6a96ad00b9c220df14f48d341c8aaa722c67859c33e93</citedby><cites>FETCH-LOGICAL-c445t-5228564f45d864f1974d6a96ad00b9c220df14f48d341c8aaa722c67859c33e93</cites><orcidid>0000-0003-0590-9101</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0021925820785169$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,3549,27924,27925,45780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11301322$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-02406676$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Moog-Lutz, Christel</creatorcontrib><creatorcontrib>Peterson, Erik J.</creatorcontrib><creatorcontrib>Lutz, Pierre G.</creatorcontrib><creatorcontrib>Eliason, Steve</creatorcontrib><creatorcontrib>Cavé-Riant, Florence</creatorcontrib><creatorcontrib>Singer, Andrew</creatorcontrib><creatorcontrib>Di Gioia, Yolande</creatorcontrib><creatorcontrib>Dmowski, Sally</creatorcontrib><creatorcontrib>Kamens, Joanne</creatorcontrib><creatorcontrib>Cayre, Yvon E.</creatorcontrib><creatorcontrib>Koretzky, Gary</creatorcontrib><title>PRAM-1 Is a Novel Adaptor Protein Regulated by Retinoic Acid (RA) and Promyelocytic Leukemia (PML)-RA Receptor α in Acute Promyelocytic Leukemia Cells</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>The t(15;17) translocation, found in 95% of acute promyelocytic leukemia, encodes a promyelocytic leukemia (PML)-retinoic acid receptor α (RARα) fusion protein. Complete remission of acute promyelocytic leukemia can be obtained by treating patients with all-trans retinoic acid, and PML-RARα plays a major role in mediating retinoic acid effects in leukemia cells. A main model proposed for acute promyelocytic leukemia is that PML-RARα exerts its oncogenic effects by repressing the expression of retinoic acid-inducible genes critical to myeloid differentiation. By applying subtraction cloning to acute promyelocytic leukemia cells, we identified a retinoic acid-induced gene, PRAM-1 (PML-RARα target gene encoding anAdaptor Molecule-1), which encodes a novel adaptor protein sharing structural homologies with the SLAP-130/fyb adaptor. PRAM-1 is expressed and regulated during normal human myelopoiesis. In U937 myeloid precursor cells, PRAM-1 expression is inhibited by expression of PML-RARα in the absence of ligand andde novo superinduced by retinoic acid. PRAM-1 associates with other adaptors, SLP-76 and SKAP-55HOM, in myeloid cell lines and with protein tyrosine kinase lyn. By providing the first evidence that PML-RARα dysregulates expression of an adaptor protein, our data open new insights into signaling events that are disrupted during transformation by PML-RARα and induced by retinoic acid duringde novo differentiation of acute promyelocytic leukemia cells.
AJ272324</description><subject>adaptor protein</subject><subject>Adaptor Proteins, Signal Transducing</subject><subject>Amino Acid Sequence</subject><subject>Base Sequence</subject><subject>Cell Differentiation</subject><subject>chromosome 15</subject><subject>chromosome 17</subject><subject>Cloning, Molecular</subject><subject>DNA, Complementary</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Humans</subject><subject>Leukemia, Promyelocytic, Acute - metabolism</subject><subject>Leukemia, Promyelocytic, Acute - pathology</subject><subject>Life Sciences</subject><subject>Molecular Sequence Data</subject><subject>Neoplasm Proteins - physiology</subject><subject>Oncogene Proteins, Fusion - physiology</subject><subject>PML-RAR^a protein</subject><subject>PRAM-1 gene</subject><subject>PRAM-1 protein</subject><subject>Proteins - chemistry</subject><subject>Proteins - genetics</subject><subject>Proteins - metabolism</subject><subject>retinoic acid receptor ^a</subject><subject>RNA, Messenger - genetics</subject><subject>Tretinoin - pharmacology</subject><subject>Tumor Cells, Cultured</subject><subject>U937 Cells</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><recordid>eNp1kUFv0zAUxy3ExLqxK0fkE1oPKX6OkzjHqAI2KYWqAmk3y7VfwSOJuzip1E_C59gX4TPhrhU7zZcn-_3eT0_-E_IO2AxYIT7er81swQBymXLGXpEJMJkmaQZ3r8mEMQ5JyTN5Ti5CuGfxiBLekHOAlEHK-YT8Wa6qRQL0NlBNv_odNrSyejv4ni57P6Dr6Ap_jo0e0NL1Pl4G13lnaGWcpderakp1Zw9su8fGm_0QezWOv7F1ml4vF_U0WVVxzOCT9O8jjcrKjAO-NDTHpglvydlGNwGvTvWS_Pj86fv8Jqm_fbmdV3VihMiGJONcZrnYiMzKWKAshM11mWvL2Lo0nDO7gdiWNhVgpNa64NzkhcxKk6ZYppdkevT-0o3a9q7V_V557dRNVavDG-OC5XmR7yCyH47stvcPI4ZBtS6YuK3u0I9BQSElByEiODuCpvch9Lj5bwamDrGpGJt6ji0OvD-Zx3WL9hk_5RQBeQQw_sXOYa-CcdgZtK5HMyjr3UvufyOjo9A</recordid><startdate>20010622</startdate><enddate>20010622</enddate><creator>Moog-Lutz, Christel</creator><creator>Peterson, Erik J.</creator><creator>Lutz, Pierre G.</creator><creator>Eliason, Steve</creator><creator>Cavé-Riant, Florence</creator><creator>Singer, Andrew</creator><creator>Di Gioia, Yolande</creator><creator>Dmowski, Sally</creator><creator>Kamens, Joanne</creator><creator>Cayre, Yvon E.</creator><creator>Koretzky, Gary</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>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0003-0590-9101</orcidid></search><sort><creationdate>20010622</creationdate><title>PRAM-1 Is a Novel Adaptor Protein Regulated by Retinoic Acid (RA) and Promyelocytic Leukemia (PML)-RA Receptor α in Acute Promyelocytic Leukemia Cells</title><author>Moog-Lutz, Christel ; Peterson, Erik J. ; Lutz, Pierre G. ; Eliason, Steve ; Cavé-Riant, Florence ; Singer, Andrew ; Di Gioia, Yolande ; Dmowski, Sally ; Kamens, Joanne ; Cayre, Yvon E. ; Koretzky, Gary</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c445t-5228564f45d864f1974d6a96ad00b9c220df14f48d341c8aaa722c67859c33e93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>adaptor protein</topic><topic>Adaptor Proteins, Signal Transducing</topic><topic>Amino Acid Sequence</topic><topic>Base Sequence</topic><topic>Cell Differentiation</topic><topic>chromosome 15</topic><topic>chromosome 17</topic><topic>Cloning, Molecular</topic><topic>DNA, Complementary</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Humans</topic><topic>Leukemia, Promyelocytic, Acute - metabolism</topic><topic>Leukemia, Promyelocytic, Acute - pathology</topic><topic>Life Sciences</topic><topic>Molecular Sequence Data</topic><topic>Neoplasm Proteins - physiology</topic><topic>Oncogene Proteins, Fusion - physiology</topic><topic>PML-RAR^a protein</topic><topic>PRAM-1 gene</topic><topic>PRAM-1 protein</topic><topic>Proteins - chemistry</topic><topic>Proteins - genetics</topic><topic>Proteins - metabolism</topic><topic>retinoic acid receptor ^a</topic><topic>RNA, Messenger - genetics</topic><topic>Tretinoin - pharmacology</topic><topic>Tumor Cells, Cultured</topic><topic>U937 Cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moog-Lutz, Christel</creatorcontrib><creatorcontrib>Peterson, Erik J.</creatorcontrib><creatorcontrib>Lutz, Pierre G.</creatorcontrib><creatorcontrib>Eliason, Steve</creatorcontrib><creatorcontrib>Cavé-Riant, Florence</creatorcontrib><creatorcontrib>Singer, Andrew</creatorcontrib><creatorcontrib>Di Gioia, Yolande</creatorcontrib><creatorcontrib>Dmowski, Sally</creatorcontrib><creatorcontrib>Kamens, Joanne</creatorcontrib><creatorcontrib>Cayre, Yvon E.</creatorcontrib><creatorcontrib>Koretzky, Gary</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>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moog-Lutz, Christel</au><au>Peterson, Erik J.</au><au>Lutz, Pierre G.</au><au>Eliason, Steve</au><au>Cavé-Riant, Florence</au><au>Singer, Andrew</au><au>Di Gioia, Yolande</au><au>Dmowski, Sally</au><au>Kamens, Joanne</au><au>Cayre, Yvon E.</au><au>Koretzky, Gary</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PRAM-1 Is a Novel Adaptor Protein Regulated by Retinoic Acid (RA) and Promyelocytic Leukemia (PML)-RA Receptor α in Acute Promyelocytic Leukemia Cells</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>2001-06-22</date><risdate>2001</risdate><volume>276</volume><issue>25</issue><spage>22375</spage><epage>22381</epage><pages>22375-22381</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>The t(15;17) translocation, found in 95% of acute promyelocytic leukemia, encodes a promyelocytic leukemia (PML)-retinoic acid receptor α (RARα) fusion protein. Complete remission of acute promyelocytic leukemia can be obtained by treating patients with all-trans retinoic acid, and PML-RARα plays a major role in mediating retinoic acid effects in leukemia cells. A main model proposed for acute promyelocytic leukemia is that PML-RARα exerts its oncogenic effects by repressing the expression of retinoic acid-inducible genes critical to myeloid differentiation. By applying subtraction cloning to acute promyelocytic leukemia cells, we identified a retinoic acid-induced gene, PRAM-1 (PML-RARα target gene encoding anAdaptor Molecule-1), which encodes a novel adaptor protein sharing structural homologies with the SLAP-130/fyb adaptor. PRAM-1 is expressed and regulated during normal human myelopoiesis. In U937 myeloid precursor cells, PRAM-1 expression is inhibited by expression of PML-RARα in the absence of ligand andde novo superinduced by retinoic acid. PRAM-1 associates with other adaptors, SLP-76 and SKAP-55HOM, in myeloid cell lines and with protein tyrosine kinase lyn. By providing the first evidence that PML-RARα dysregulates expression of an adaptor protein, our data open new insights into signaling events that are disrupted during transformation by PML-RARα and induced by retinoic acid duringde novo differentiation of acute promyelocytic leukemia cells.
AJ272324</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>11301322</pmid><doi>10.1074/jbc.M011683200</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0003-0590-9101</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | adaptor protein Adaptor Proteins, Signal Transducing Amino Acid Sequence Base Sequence Cell Differentiation chromosome 15 chromosome 17 Cloning, Molecular DNA, Complementary Gene Expression Regulation, Neoplastic - drug effects Humans Leukemia, Promyelocytic, Acute - metabolism Leukemia, Promyelocytic, Acute - pathology Life Sciences Molecular Sequence Data Neoplasm Proteins - physiology Oncogene Proteins, Fusion - physiology PML-RAR^a protein PRAM-1 gene PRAM-1 protein Proteins - chemistry Proteins - genetics Proteins - metabolism retinoic acid receptor ^a RNA, Messenger - genetics Tretinoin - pharmacology Tumor Cells, Cultured U937 Cells |
| title | PRAM-1 Is a Novel Adaptor Protein Regulated by Retinoic Acid (RA) and Promyelocytic Leukemia (PML)-RA Receptor α in Acute Promyelocytic Leukemia Cells |
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