HOXB4 confers a constant rate of in vitro proliferation to transduced bone marrow cells
HOXB4 overexpression mediates increased self-renewal of haematopoietic stem cells (HSCs) ex vivo . Since HOXB4-expanded HSCs retain normal differentiation potential and there is no leukaemia development from transduced HSCs, HOXB4 represents a promising tool for human HSC therapy. However, the incre...
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| Veröffentlicht in: | Oncogene 2005-01, Vol.24 (4), p.561-572 |
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| creator | Schmittwolf, Carolin Porsch, Matthias Greiner, Axel Avots, Andris Müller, Albrecht M |
| description | HOXB4 overexpression mediates increased self-renewal of haematopoietic stem cells (HSCs)
ex vivo
. Since HOXB4-expanded HSCs retain normal differentiation potential and there is no leukaemia development from transduced HSCs, HOXB4 represents a promising tool for human HSC therapy. However, the increased proliferation capacity of HOXB4 overexpressing fibroblasts resulting from upregulation of JunB, Fra-1 and cyclin D1 protein levels may indicate a potential risk associated with the HOXB4 overexpression approach. This prompted us to investigate the proliferation rate, differentiation and expression of cell cycle regulators directly in bone marrow cultures overexpressing HOXB4. Here we show that in comparison to neo-transduced control bone marrow cultures, HOXB4-overexpressing cultures had a more homogenous morphology and increased numbers of haematopoietic progenitor cells capable to generate primitive colonies
in vitro
. In contrast, neo-transduced bone marrow cells in long-term cultures showed hallmarks of myeloid differentiation and a reduced secondary colony forming activity. We further show that multilineage repopulating activity
in vivo
, which was present only in HOXB4 long-term cultures, declined over time. HOXB4 overexpression
in vitro
did not result in an increase but in a stabilization of the proliferation rate (1.4–1.8 cell divisions per day), while the proliferation rate of control neo-transduced bone marrow cultures gradually declined. Correspondingly, increased HOXB4 expression was paralleled by decreased expression levels of cyclins, CDKs and AP-1 family members. These results suggest that the growth rate of HOXB4- compared to neo-transduced bone marrow cells remains constant in long-term cultures along with a suppression of myeloid differentiation. In contrast to HOXB4 overexpression in fibroblasts, bone marrow cells engineered to overexpress HOXB4 do not upregulate AP-1 complex members or cyclins indicating that HOXB4 acts in a cell type-specific way. |
| doi_str_mv | 10.1038/sj.onc.1208202 |
| format | Article |
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ex vivo
. Since HOXB4-expanded HSCs retain normal differentiation potential and there is no leukaemia development from transduced HSCs, HOXB4 represents a promising tool for human HSC therapy. However, the increased proliferation capacity of HOXB4 overexpressing fibroblasts resulting from upregulation of JunB, Fra-1 and cyclin D1 protein levels may indicate a potential risk associated with the HOXB4 overexpression approach. This prompted us to investigate the proliferation rate, differentiation and expression of cell cycle regulators directly in bone marrow cultures overexpressing HOXB4. Here we show that in comparison to neo-transduced control bone marrow cultures, HOXB4-overexpressing cultures had a more homogenous morphology and increased numbers of haematopoietic progenitor cells capable to generate primitive colonies
in vitro
. In contrast, neo-transduced bone marrow cells in long-term cultures showed hallmarks of myeloid differentiation and a reduced secondary colony forming activity. We further show that multilineage repopulating activity
in vivo
, which was present only in HOXB4 long-term cultures, declined over time. HOXB4 overexpression
in vitro
did not result in an increase but in a stabilization of the proliferation rate (1.4–1.8 cell divisions per day), while the proliferation rate of control neo-transduced bone marrow cultures gradually declined. Correspondingly, increased HOXB4 expression was paralleled by decreased expression levels of cyclins, CDKs and AP-1 family members. These results suggest that the growth rate of HOXB4- compared to neo-transduced bone marrow cells remains constant in long-term cultures along with a suppression of myeloid differentiation. In contrast to HOXB4 overexpression in fibroblasts, bone marrow cells engineered to overexpress HOXB4 do not upregulate AP-1 complex members or cyclins indicating that HOXB4 acts in a cell type-specific way.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1208202</identifier><identifier>PMID: 15580301</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Animals ; Apoptosis ; Biological and medical sciences ; Bone marrow ; Bone Marrow Cells - cytology ; Bone Marrow Cells - metabolism ; Bone Marrow Transplantation ; Cell Biology ; Cell cycle ; Cell Differentiation - genetics ; Cell physiology ; Cell Proliferation ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Cells, Cultured ; Cyclin-Dependent Kinases - genetics ; Cyclins - genetics ; Fundamental and applied biological sciences. Psychology ; Homeodomain Proteins - genetics ; Homeodomain Proteins - metabolism ; Human Genetics ; Internal Medicine ; Leukemia ; Medicine ; Medicine & Public Health ; Mice ; Molecular and cellular biology ; Oncology ; original-paper ; Pathology ; Proteins ; Stem cells ; Transcription Factor AP-1 - genetics ; Transcription Factors ; Transcription, Genetic ; Transduction, Genetic</subject><ispartof>Oncogene, 2005-01, Vol.24 (4), p.561-572</ispartof><rights>Springer Nature Limited 2005</rights><rights>2005 INIST-CNRS</rights><rights>COPYRIGHT 2005 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jan 20, 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-66469f2a9bc045fe47dbd876cb7ab4d3ffcb921dff73ba13d6aea161736c5c763</citedby><cites>FETCH-LOGICAL-c526t-66469f2a9bc045fe47dbd876cb7ab4d3ffcb921dff73ba13d6aea161736c5c763</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.1208202$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.onc.1208202$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16480282$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15580301$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schmittwolf, Carolin</creatorcontrib><creatorcontrib>Porsch, Matthias</creatorcontrib><creatorcontrib>Greiner, Axel</creatorcontrib><creatorcontrib>Avots, Andris</creatorcontrib><creatorcontrib>Müller, Albrecht M</creatorcontrib><title>HOXB4 confers a constant rate of in vitro proliferation to transduced bone marrow cells</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>HOXB4 overexpression mediates increased self-renewal of haematopoietic stem cells (HSCs)
ex vivo
. Since HOXB4-expanded HSCs retain normal differentiation potential and there is no leukaemia development from transduced HSCs, HOXB4 represents a promising tool for human HSC therapy. However, the increased proliferation capacity of HOXB4 overexpressing fibroblasts resulting from upregulation of JunB, Fra-1 and cyclin D1 protein levels may indicate a potential risk associated with the HOXB4 overexpression approach. This prompted us to investigate the proliferation rate, differentiation and expression of cell cycle regulators directly in bone marrow cultures overexpressing HOXB4. Here we show that in comparison to neo-transduced control bone marrow cultures, HOXB4-overexpressing cultures had a more homogenous morphology and increased numbers of haematopoietic progenitor cells capable to generate primitive colonies
in vitro
. In contrast, neo-transduced bone marrow cells in long-term cultures showed hallmarks of myeloid differentiation and a reduced secondary colony forming activity. We further show that multilineage repopulating activity
in vivo
, which was present only in HOXB4 long-term cultures, declined over time. HOXB4 overexpression
in vitro
did not result in an increase but in a stabilization of the proliferation rate (1.4–1.8 cell divisions per day), while the proliferation rate of control neo-transduced bone marrow cultures gradually declined. Correspondingly, increased HOXB4 expression was paralleled by decreased expression levels of cyclins, CDKs and AP-1 family members. These results suggest that the growth rate of HOXB4- compared to neo-transduced bone marrow cells remains constant in long-term cultures along with a suppression of myeloid differentiation. In contrast to HOXB4 overexpression in fibroblasts, bone marrow cells engineered to overexpress HOXB4 do not upregulate AP-1 complex members or cyclins indicating that HOXB4 acts in a cell type-specific way.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Bone marrow</subject><subject>Bone Marrow Cells - cytology</subject><subject>Bone Marrow Cells - metabolism</subject><subject>Bone Marrow Transplantation</subject><subject>Cell Biology</subject><subject>Cell cycle</subject><subject>Cell Differentiation - genetics</subject><subject>Cell physiology</subject><subject>Cell Proliferation</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Cells, Cultured</subject><subject>Cyclin-Dependent Kinases - genetics</subject><subject>Cyclins - genetics</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Homeodomain Proteins - genetics</subject><subject>Homeodomain Proteins - metabolism</subject><subject>Human Genetics</subject><subject>Internal Medicine</subject><subject>Leukemia</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Molecular and cellular biology</subject><subject>Oncology</subject><subject>original-paper</subject><subject>Pathology</subject><subject>Proteins</subject><subject>Stem cells</subject><subject>Transcription Factor AP-1 - genetics</subject><subject>Transcription Factors</subject><subject>Transcription, Genetic</subject><subject>Transduction, Genetic</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</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>eNqFkcuLFDEQxoMo7rh69ShBcG89m_fjuC6uKyzsRdFbSOexZOhJ1qRb8b834zQMCCI5JFR-VfVVfQC8xmiLEVWXbbct2W0xQYog8gRsMJNi4Fyzp2CDNEeDJpScgRet7RBCUiPyHJxhzhWiCG_A19v7b-8ZdCXHUBu0h1ebbZ5htXOAJcKU4Y801wIfa5lSp-ycSoZzgXO1ufnFBQ_HkgPc21rLT-jCNLWX4Fm0Uwuv1vscfLn58Pn6dri7__jp-upucJyIeRCCCR2J1aNDjMfApB-9ksKN0o7M0xjdqAn2MUo6Wky9sMFigSUVjjsp6Dm4ONbt6r4voc1mn9pBgc2hLM2ITjIt5X9BLBVCRKoOvv0L3JWl5j6EIURSjohiHdoeoQc7BZNyLH0Zrh8f9qmvMMTU41dYadRH_NN-TXC1tFZDNI819YX9MhiZg5Om7Ux30qxO9oQ3q4xl3Ad_wlfrOvBuBWxzdordDJfaiRNMdamHQpdHrvWv_BDqaZ5_tP4NXwS2Xw</recordid><startdate>20050120</startdate><enddate>20050120</enddate><creator>Schmittwolf, Carolin</creator><creator>Porsch, Matthias</creator><creator>Greiner, Axel</creator><creator>Avots, Andris</creator><creator>Müller, Albrecht M</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>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20050120</creationdate><title>HOXB4 confers a constant rate of in vitro proliferation to transduced bone marrow cells</title><author>Schmittwolf, Carolin ; Porsch, Matthias ; Greiner, Axel ; Avots, Andris ; Müller, Albrecht M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-66469f2a9bc045fe47dbd876cb7ab4d3ffcb921dff73ba13d6aea161736c5c763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Bone marrow</topic><topic>Bone Marrow Cells - cytology</topic><topic>Bone Marrow Cells - metabolism</topic><topic>Bone Marrow Transplantation</topic><topic>Cell Biology</topic><topic>Cell cycle</topic><topic>Cell Differentiation - genetics</topic><topic>Cell physiology</topic><topic>Cell Proliferation</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Cells, Cultured</topic><topic>Cyclin-Dependent Kinases - genetics</topic><topic>Cyclins - genetics</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Homeodomain Proteins - genetics</topic><topic>Homeodomain Proteins - metabolism</topic><topic>Human Genetics</topic><topic>Internal Medicine</topic><topic>Leukemia</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Molecular and cellular biology</topic><topic>Oncology</topic><topic>original-paper</topic><topic>Pathology</topic><topic>Proteins</topic><topic>Stem cells</topic><topic>Transcription Factor AP-1 - genetics</topic><topic>Transcription Factors</topic><topic>Transcription, Genetic</topic><topic>Transduction, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schmittwolf, Carolin</creatorcontrib><creatorcontrib>Porsch, Matthias</creatorcontrib><creatorcontrib>Greiner, Axel</creatorcontrib><creatorcontrib>Avots, Andris</creatorcontrib><creatorcontrib>Müller, Albrecht M</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 China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schmittwolf, Carolin</au><au>Porsch, Matthias</au><au>Greiner, Axel</au><au>Avots, Andris</au><au>Müller, Albrecht M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HOXB4 confers a constant rate of in vitro proliferation to transduced bone marrow cells</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2005-01-20</date><risdate>2005</risdate><volume>24</volume><issue>4</issue><spage>561</spage><epage>572</epage><pages>561-572</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>HOXB4 overexpression mediates increased self-renewal of haematopoietic stem cells (HSCs)
ex vivo
. Since HOXB4-expanded HSCs retain normal differentiation potential and there is no leukaemia development from transduced HSCs, HOXB4 represents a promising tool for human HSC therapy. However, the increased proliferation capacity of HOXB4 overexpressing fibroblasts resulting from upregulation of JunB, Fra-1 and cyclin D1 protein levels may indicate a potential risk associated with the HOXB4 overexpression approach. This prompted us to investigate the proliferation rate, differentiation and expression of cell cycle regulators directly in bone marrow cultures overexpressing HOXB4. Here we show that in comparison to neo-transduced control bone marrow cultures, HOXB4-overexpressing cultures had a more homogenous morphology and increased numbers of haematopoietic progenitor cells capable to generate primitive colonies
in vitro
. In contrast, neo-transduced bone marrow cells in long-term cultures showed hallmarks of myeloid differentiation and a reduced secondary colony forming activity. We further show that multilineage repopulating activity
in vivo
, which was present only in HOXB4 long-term cultures, declined over time. HOXB4 overexpression
in vitro
did not result in an increase but in a stabilization of the proliferation rate (1.4–1.8 cell divisions per day), while the proliferation rate of control neo-transduced bone marrow cultures gradually declined. Correspondingly, increased HOXB4 expression was paralleled by decreased expression levels of cyclins, CDKs and AP-1 family members. These results suggest that the growth rate of HOXB4- compared to neo-transduced bone marrow cells remains constant in long-term cultures along with a suppression of myeloid differentiation. In contrast to HOXB4 overexpression in fibroblasts, bone marrow cells engineered to overexpress HOXB4 do not upregulate AP-1 complex members or cyclins indicating that HOXB4 acts in a cell type-specific way.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>15580301</pmid><doi>10.1038/sj.onc.1208202</doi><tpages>12</tpages></addata></record> |
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| ispartof | Oncogene, 2005-01, Vol.24 (4), p.561-572 |
| issn | 0950-9232 1476-5594 |
| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Nature Journals Online; SpringerLink Journals - AutoHoldings |
| subjects | Animals Apoptosis Biological and medical sciences Bone marrow Bone Marrow Cells - cytology Bone Marrow Cells - metabolism Bone Marrow Transplantation Cell Biology Cell cycle Cell Differentiation - genetics Cell physiology Cell Proliferation Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cells, Cultured Cyclin-Dependent Kinases - genetics Cyclins - genetics Fundamental and applied biological sciences. Psychology Homeodomain Proteins - genetics Homeodomain Proteins - metabolism Human Genetics Internal Medicine Leukemia Medicine Medicine & Public Health Mice Molecular and cellular biology Oncology original-paper Pathology Proteins Stem cells Transcription Factor AP-1 - genetics Transcription Factors Transcription, Genetic Transduction, Genetic |
| title | HOXB4 confers a constant rate of in vitro proliferation to transduced bone marrow cells |
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