A pathway from leukemogenic oncogenes and stem cell chemokines to RNA processing via THOC5
THOC5 is a member of the THO complex that is involved in processing and transport of mRNA. We have shown previously that hematopoietic stem cells have an absolute requirement for THOC5 for survival and that THOC5 is phosphorylated on tyrosine 225 as a consequence of leukemogenic protein tyrosine kin...
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| Veröffentlicht in: | Leukemia 2013-04, Vol.27 (4), p.932-940 |
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| creator | Griaud, F Pierce, A Gonzalez Sanchez, M B Scott, M Abraham, S A Holyoake, T L Tran, D D H Tamura, T Whetton, A D |
| description | THOC5 is a member of the THO complex that is involved in processing and transport of mRNA. We have shown previously that hematopoietic stem cells have an absolute requirement for THOC5 for survival and that THOC5 is phosphorylated on tyrosine 225 as a consequence of leukemogenic protein tyrosine kinase (PTK) action. We have investigated pathways for THOC5 phosphorylation to develop an understanding of THO complex modulation by tyrosine kinase (TK) oncogenes in leukemias. We demonstrate that THOC5 phosphorylation is mediated by Src PTK and CD45 protein tyrosine phosphatase action and that this event is sensitive to oxidative status. We show that THOC5 phosphorylation is elevated in stem cells from patients with chronic myeloid leukemia (CML) and that this phosphorylation is sensitive to the frontline drugs used in CML treatment. Further we show that THOC5 Y225 phosphorylation governs mRNA binding. In addition, CXCL12 is shown to induce THOC5 Y225 phosphorylation, and site-directed mutagenesis demonstrates that this modulates motile response. In conclusion, we delineate a signaling pathway stimulated by leukemogenic PTKs, chemokines and oxidative stress that can affect THO complex mediation of gene expression describing mechanisms for post-transcriptional regulation of protein levels. |
| doi_str_mv | 10.1038/leu.2012.283 |
| format | Article |
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We have shown previously that hematopoietic stem cells have an absolute requirement for THOC5 for survival and that THOC5 is phosphorylated on tyrosine 225 as a consequence of leukemogenic protein tyrosine kinase (PTK) action. We have investigated pathways for THOC5 phosphorylation to develop an understanding of THO complex modulation by tyrosine kinase (TK) oncogenes in leukemias. We demonstrate that THOC5 phosphorylation is mediated by Src PTK and CD45 protein tyrosine phosphatase action and that this event is sensitive to oxidative status. We show that THOC5 phosphorylation is elevated in stem cells from patients with chronic myeloid leukemia (CML) and that this phosphorylation is sensitive to the frontline drugs used in CML treatment. Further we show that THOC5 Y225 phosphorylation governs mRNA binding. In addition, CXCL12 is shown to induce THOC5 Y225 phosphorylation, and site-directed mutagenesis demonstrates that this modulates motile response. In conclusion, we delineate a signaling pathway stimulated by leukemogenic PTKs, chemokines and oxidative stress that can affect THO complex mediation of gene expression describing mechanisms for post-transcriptional regulation of protein levels.</description><identifier>ISSN: 0887-6924</identifier><identifier>EISSN: 1476-5551</identifier><identifier>DOI: 10.1038/leu.2012.283</identifier><identifier>PMID: 23032722</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/337/1645 ; 631/80/304 ; 631/80/86 ; 692/699/67/1990/283/1896 ; Cancer Research ; CD45 antigen ; Chemokines ; Chemokines - metabolism ; Chronic myeloid leukemia ; Critical Care Medicine ; CXCL12 protein ; Gene expression ; Gene mutations ; Gene regulation ; Heat shock proteins ; Hematology ; Hematopoietic stem cells ; Humans ; Immunohistochemistry ; Intensive ; Internal Medicine ; Kinases ; Leukemia ; Leukemia - genetics ; Medicine ; Medicine & Public Health ; Motility ; Myeloid leukemia ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Oncogenes ; Oncology ; original-article ; Oxidative stress ; Phosphatase ; Phosphorylation ; Physiological aspects ; Post-transcription ; Protein-tyrosine kinase ; Protein-tyrosine-phosphatase ; Proteins ; Proteomics ; RNA processing ; RNA Processing, Post-Transcriptional ; RNA transport ; Signal Transduction ; Site-directed mutagenesis ; Stem cells ; Stem Cells - metabolism ; Transcription factors ; Tyrosine ; Tyrosine - metabolism</subject><ispartof>Leukemia, 2013-04, Vol.27 (4), p.932-940</ispartof><rights>Macmillan Publishers Limited 2013</rights><rights>COPYRIGHT 2013 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Apr 2013</rights><rights>Macmillan Publishers Limited 2013.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c516t-1af569719fc3a7d07d286dbadfbc14639c56756814753158cfa0ef0f81d05edf3</citedby><cites>FETCH-LOGICAL-c516t-1af569719fc3a7d07d286dbadfbc14639c56756814753158cfa0ef0f81d05edf3</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/leu.2012.283$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/leu.2012.283$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23032722$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Griaud, F</creatorcontrib><creatorcontrib>Pierce, A</creatorcontrib><creatorcontrib>Gonzalez Sanchez, M B</creatorcontrib><creatorcontrib>Scott, M</creatorcontrib><creatorcontrib>Abraham, S A</creatorcontrib><creatorcontrib>Holyoake, T L</creatorcontrib><creatorcontrib>Tran, D D H</creatorcontrib><creatorcontrib>Tamura, T</creatorcontrib><creatorcontrib>Whetton, A D</creatorcontrib><title>A pathway from leukemogenic oncogenes and stem cell chemokines to RNA processing via THOC5</title><title>Leukemia</title><addtitle>Leukemia</addtitle><addtitle>Leukemia</addtitle><description>THOC5 is a member of the THO complex that is involved in processing and transport of mRNA. We have shown previously that hematopoietic stem cells have an absolute requirement for THOC5 for survival and that THOC5 is phosphorylated on tyrosine 225 as a consequence of leukemogenic protein tyrosine kinase (PTK) action. We have investigated pathways for THOC5 phosphorylation to develop an understanding of THO complex modulation by tyrosine kinase (TK) oncogenes in leukemias. We demonstrate that THOC5 phosphorylation is mediated by Src PTK and CD45 protein tyrosine phosphatase action and that this event is sensitive to oxidative status. We show that THOC5 phosphorylation is elevated in stem cells from patients with chronic myeloid leukemia (CML) and that this phosphorylation is sensitive to the frontline drugs used in CML treatment. Further we show that THOC5 Y225 phosphorylation governs mRNA binding. In addition, CXCL12 is shown to induce THOC5 Y225 phosphorylation, and site-directed mutagenesis demonstrates that this modulates motile response. In conclusion, we delineate a signaling pathway stimulated by leukemogenic PTKs, chemokines and oxidative stress that can affect THO complex mediation of gene expression describing mechanisms for post-transcriptional regulation of protein levels.</description><subject>631/337/1645</subject><subject>631/80/304</subject><subject>631/80/86</subject><subject>692/699/67/1990/283/1896</subject><subject>Cancer Research</subject><subject>CD45 antigen</subject><subject>Chemokines</subject><subject>Chemokines - metabolism</subject><subject>Chronic myeloid leukemia</subject><subject>Critical Care Medicine</subject><subject>CXCL12 protein</subject><subject>Gene expression</subject><subject>Gene mutations</subject><subject>Gene regulation</subject><subject>Heat shock proteins</subject><subject>Hematology</subject><subject>Hematopoietic stem cells</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Intensive</subject><subject>Internal Medicine</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Leukemia - 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metabolism</topic><topic>Transcription factors</topic><topic>Tyrosine</topic><topic>Tyrosine - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Griaud, F</creatorcontrib><creatorcontrib>Pierce, A</creatorcontrib><creatorcontrib>Gonzalez Sanchez, M B</creatorcontrib><creatorcontrib>Scott, M</creatorcontrib><creatorcontrib>Abraham, S A</creatorcontrib><creatorcontrib>Holyoake, T L</creatorcontrib><creatorcontrib>Tran, D D H</creatorcontrib><creatorcontrib>Tamura, T</creatorcontrib><creatorcontrib>Whetton, A D</creatorcontrib><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>Bacteriology Abstracts (Microbiology B)</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</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>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>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>Environmental Sciences and Pollution Management</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>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</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 China</collection><jtitle>Leukemia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Griaud, F</au><au>Pierce, A</au><au>Gonzalez Sanchez, M B</au><au>Scott, M</au><au>Abraham, S A</au><au>Holyoake, T L</au><au>Tran, D D H</au><au>Tamura, T</au><au>Whetton, A D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A pathway from leukemogenic oncogenes and stem cell chemokines to RNA processing via THOC5</atitle><jtitle>Leukemia</jtitle><stitle>Leukemia</stitle><addtitle>Leukemia</addtitle><date>2013-04-01</date><risdate>2013</risdate><volume>27</volume><issue>4</issue><spage>932</spage><epage>940</epage><pages>932-940</pages><issn>0887-6924</issn><eissn>1476-5551</eissn><abstract>THOC5 is a member of the THO complex that is involved in processing and transport of mRNA. We have shown previously that hematopoietic stem cells have an absolute requirement for THOC5 for survival and that THOC5 is phosphorylated on tyrosine 225 as a consequence of leukemogenic protein tyrosine kinase (PTK) action. We have investigated pathways for THOC5 phosphorylation to develop an understanding of THO complex modulation by tyrosine kinase (TK) oncogenes in leukemias. We demonstrate that THOC5 phosphorylation is mediated by Src PTK and CD45 protein tyrosine phosphatase action and that this event is sensitive to oxidative status. We show that THOC5 phosphorylation is elevated in stem cells from patients with chronic myeloid leukemia (CML) and that this phosphorylation is sensitive to the frontline drugs used in CML treatment. Further we show that THOC5 Y225 phosphorylation governs mRNA binding. In addition, CXCL12 is shown to induce THOC5 Y225 phosphorylation, and site-directed mutagenesis demonstrates that this modulates motile response. In conclusion, we delineate a signaling pathway stimulated by leukemogenic PTKs, chemokines and oxidative stress that can affect THO complex mediation of gene expression describing mechanisms for post-transcriptional regulation of protein levels.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>23032722</pmid><doi>10.1038/leu.2012.283</doi><tpages>9</tpages></addata></record> |
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| source | MEDLINE; Springer Nature - Complete Springer Journals; Nature Journals Online; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | 631/337/1645 631/80/304 631/80/86 692/699/67/1990/283/1896 Cancer Research CD45 antigen Chemokines Chemokines - metabolism Chronic myeloid leukemia Critical Care Medicine CXCL12 protein Gene expression Gene mutations Gene regulation Heat shock proteins Hematology Hematopoietic stem cells Humans Immunohistochemistry Intensive Internal Medicine Kinases Leukemia Leukemia - genetics Medicine Medicine & Public Health Motility Myeloid leukemia Nuclear Proteins - genetics Nuclear Proteins - metabolism Oncogenes Oncology original-article Oxidative stress Phosphatase Phosphorylation Physiological aspects Post-transcription Protein-tyrosine kinase Protein-tyrosine-phosphatase Proteins Proteomics RNA processing RNA Processing, Post-Transcriptional RNA transport Signal Transduction Site-directed mutagenesis Stem cells Stem Cells - metabolism Transcription factors Tyrosine Tyrosine - metabolism |
| title | A pathway from leukemogenic oncogenes and stem cell chemokines to RNA processing via THOC5 |
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