Thrombopoietin-induced conformational change in p53 lies downstream of the p44/p42 mitogen activated protein kinase cascade in the human growth factor-dependent cell line M07e
Thrombopoietin is a cytokine with potent megakaryocytopoietic and thrombopoietic activities in vivo. Wild-type p53 is a conformationally flexible, anti-oncogenic transcription factor that plays a principal role in mediating growth factor withdrawal-induced apoptosis in factor-dependent hematopoietic...
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| Veröffentlicht in: | Oncogene 1999-02, Vol.18 (7), p.1465-1477 |
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| creator | RITCHIE, A BRAUN, S. E HE, J BROXMEYER, H. E |
| description | Thrombopoietin is a cytokine with potent megakaryocytopoietic and thrombopoietic activities in vivo. Wild-type p53 is a conformationally flexible, anti-oncogenic transcription factor that plays a principal role in mediating growth factor withdrawal-induced apoptosis in factor-dependent hematopoietic cells. We recently reported that Tpo induces a conformational change in and functional inactivation of p53, coincident with its anti-apoptotic effects, in the human factor-dependent cell line M07e. In an effort to identify potential signaling cascades through which Tpo illicits these effects on p53, we report here that treating M07e cells with MAPK kinase inhibitor PD98059 dramatically suppressed Tpo-induced conformational change in p53 as well as Tpo-enhanced viability in M07e cells in a p53-dependent manner. Furthermore, the expression of constitutively active Raf1 in M07e cells induced conformational change in p53 independent of Tpo stimulation. Inhibition of the JAK/STAT pathway revealed that JAK/STAT signaling plays an insignificant role in conformational modulation of p53 and apoptosis suppression. Inhibition of phosphatidylinositol-3 kinase did not have a significant effect on p53 conformation but did have a weak but significant effect on Tpo-enhanced viability. Cytokine-induced activation of the MAPK pathway and the subsequent functional neutralization of p53, may be an event by which apoptosis is commonly suppressed in hematopoiesis. |
| doi_str_mv | 10.1038/sj.onc.1202439 |
| format | Article |
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E ; HE, J ; BROXMEYER, H. E</creator><creatorcontrib>RITCHIE, A ; BRAUN, S. E ; HE, J ; BROXMEYER, H. E</creatorcontrib><description>Thrombopoietin is a cytokine with potent megakaryocytopoietic and thrombopoietic activities in vivo. Wild-type p53 is a conformationally flexible, anti-oncogenic transcription factor that plays a principal role in mediating growth factor withdrawal-induced apoptosis in factor-dependent hematopoietic cells. We recently reported that Tpo induces a conformational change in and functional inactivation of p53, coincident with its anti-apoptotic effects, in the human factor-dependent cell line M07e. In an effort to identify potential signaling cascades through which Tpo illicits these effects on p53, we report here that treating M07e cells with MAPK kinase inhibitor PD98059 dramatically suppressed Tpo-induced conformational change in p53 as well as Tpo-enhanced viability in M07e cells in a p53-dependent manner. Furthermore, the expression of constitutively active Raf1 in M07e cells induced conformational change in p53 independent of Tpo stimulation. Inhibition of the JAK/STAT pathway revealed that JAK/STAT signaling plays an insignificant role in conformational modulation of p53 and apoptosis suppression. Inhibition of phosphatidylinositol-3 kinase did not have a significant effect on p53 conformation but did have a weak but significant effect on Tpo-enhanced viability. Cytokine-induced activation of the MAPK pathway and the subsequent functional neutralization of p53, may be an event by which apoptosis is commonly suppressed in hematopoiesis.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1202439</identifier><identifier>PMID: 10050883</identifier><language>eng</language><publisher>Basingstoke: Nature Publishing</publisher><subject>1-Phosphatidylinositol 3-kinase ; Ageing, cell death ; Animals ; Anti-oncogenes ; Apoptosis ; Biological and medical sciences ; Calcium-Calmodulin-Dependent Protein Kinases - antagonists & inhibitors ; Calcium-Calmodulin-Dependent Protein Kinases - metabolism ; Cell Line ; Cell physiology ; Cell Survival ; Cytokines ; DNA-Binding Proteins - antagonists & inhibitors ; DNA-Binding Proteins - metabolism ; Enzyme Activation ; Enzyme inhibitors ; Enzyme Inhibitors - pharmacology ; Flavonoids - pharmacology ; Fundamental and applied biological sciences. Psychology ; Genotype ; Granulocyte-Macrophage Colony-Stimulating Factor - metabolism ; Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology ; Growth factors ; Humans ; Janus Kinase 2 ; Kinases ; MAP kinase ; Mice ; Milk Proteins ; Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinases ; Molecular and cellular biology ; p53 Protein ; Phosphatidylinositol 3-Kinases - metabolism ; Promoter Regions, Genetic ; Protein Conformation ; Protein kinase ; Protein kinase C ; Protein-Tyrosine Kinases - antagonists & inhibitors ; Protein-Tyrosine Kinases - metabolism ; Proto-Oncogene Proteins ; Signal transduction ; STAT5 Transcription Factor ; Thrombopoietin ; Thrombopoietin - pharmacology ; Time Factors ; Trans-Activators - antagonists & inhibitors ; Trans-Activators - metabolism ; Tumor Suppressor Protein p53 - chemistry ; Tumor Suppressor Protein p53 - genetics ; Up-Regulation</subject><ispartof>Oncogene, 1999-02, Vol.18 (7), p.1465-1477</ispartof><rights>1999 INIST-CNRS</rights><rights>Macmillan Publishers Limited 1999.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c379t-433bb6c3987777d1674c15aa95a2570d3e7718f46d1182c70a264656e22a74c33</citedby><cites>FETCH-LOGICAL-c379t-433bb6c3987777d1674c15aa95a2570d3e7718f46d1182c70a264656e22a74c33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1721058$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10050883$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>RITCHIE, A</creatorcontrib><creatorcontrib>BRAUN, S. E</creatorcontrib><creatorcontrib>HE, J</creatorcontrib><creatorcontrib>BROXMEYER, H. E</creatorcontrib><title>Thrombopoietin-induced conformational change in p53 lies downstream of the p44/p42 mitogen activated protein kinase cascade in the human growth factor-dependent cell line M07e</title><title>Oncogene</title><addtitle>Oncogene</addtitle><description>Thrombopoietin is a cytokine with potent megakaryocytopoietic and thrombopoietic activities in vivo. Wild-type p53 is a conformationally flexible, anti-oncogenic transcription factor that plays a principal role in mediating growth factor withdrawal-induced apoptosis in factor-dependent hematopoietic cells. We recently reported that Tpo induces a conformational change in and functional inactivation of p53, coincident with its anti-apoptotic effects, in the human factor-dependent cell line M07e. In an effort to identify potential signaling cascades through which Tpo illicits these effects on p53, we report here that treating M07e cells with MAPK kinase inhibitor PD98059 dramatically suppressed Tpo-induced conformational change in p53 as well as Tpo-enhanced viability in M07e cells in a p53-dependent manner. Furthermore, the expression of constitutively active Raf1 in M07e cells induced conformational change in p53 independent of Tpo stimulation. Inhibition of the JAK/STAT pathway revealed that JAK/STAT signaling plays an insignificant role in conformational modulation of p53 and apoptosis suppression. Inhibition of phosphatidylinositol-3 kinase did not have a significant effect on p53 conformation but did have a weak but significant effect on Tpo-enhanced viability. Cytokine-induced activation of the MAPK pathway and the subsequent functional neutralization of p53, may be an event by which apoptosis is commonly suppressed in hematopoiesis.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Ageing, cell death</subject><subject>Animals</subject><subject>Anti-oncogenes</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Calcium-Calmodulin-Dependent Protein Kinases - antagonists & inhibitors</subject><subject>Calcium-Calmodulin-Dependent Protein Kinases - metabolism</subject><subject>Cell Line</subject><subject>Cell physiology</subject><subject>Cell Survival</subject><subject>Cytokines</subject><subject>DNA-Binding Proteins - antagonists & inhibitors</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Enzyme Activation</subject><subject>Enzyme inhibitors</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Flavonoids - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genotype</subject><subject>Granulocyte-Macrophage Colony-Stimulating Factor - metabolism</subject><subject>Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Janus Kinase 2</subject><subject>Kinases</subject><subject>MAP kinase</subject><subject>Mice</subject><subject>Milk Proteins</subject><subject>Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3</subject><subject>Mitogen-Activated Protein Kinases</subject><subject>Molecular and cellular biology</subject><subject>p53 Protein</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Promoter Regions, Genetic</subject><subject>Protein Conformation</subject><subject>Protein kinase</subject><subject>Protein kinase C</subject><subject>Protein-Tyrosine Kinases - antagonists & inhibitors</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>Proto-Oncogene Proteins</subject><subject>Signal transduction</subject><subject>STAT5 Transcription Factor</subject><subject>Thrombopoietin</subject><subject>Thrombopoietin - pharmacology</subject><subject>Time Factors</subject><subject>Trans-Activators - antagonists & inhibitors</subject><subject>Trans-Activators - metabolism</subject><subject>Tumor Suppressor Protein p53 - chemistry</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Up-Regulation</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u1DAUhSMEokNhyxJZAnWXqf8dL1EFBamITVlHHvtmxkNiB9uh4ql4RRxmJBAbvLkLf-fcq3Oa5iXBW4JZd52P2xjsllBMOdOPmg3hSrZCaP642WAtcKspoxfNs5yPGGOlMX3aXBCMBe46tml-3h9SnHZxjh6KD60PbrHgkI1hiGkyxcdgRmQPJuwB-YBmwdDoISMXH0IuCcyE4oDKAdDM-fXMKZp8iXsIyNjiv5tS3eYUC1TxVx9MBmRNtsb9tlt1h2UyAe1TfCgHNFRVTK2DGYKDUJCFcawbA6BPWMHz5slgxgwvzvOy-fL-3f3Nh_bu8-3Hm7d3rWVKl5YztttJy3Sn6nNEKm6JMEYLQ4XCjoFSpBu4dIR01CpsqORSSKDUVJSxy-bq5FtP_7ZALv3k83qKCRCX3EtdI1Za_xckimgtOang63_AY1xSDTf3dP2vBcrVbnuibIo5Jxj6OfnJpB89wf3aeJ-PfW28PzdeBa_OtstuAvcXfqq4Am_OwJr6OCQTrM9_OEUJFh37BV7BtL0</recordid><startdate>19990218</startdate><enddate>19990218</enddate><creator>RITCHIE, A</creator><creator>BRAUN, S. E</creator><creator>HE, J</creator><creator>BROXMEYER, H. E</creator><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>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>19990218</creationdate><title>Thrombopoietin-induced conformational change in p53 lies downstream of the p44/p42 mitogen activated protein kinase cascade in the human growth factor-dependent cell line M07e</title><author>RITCHIE, A ; BRAUN, S. E ; HE, J ; BROXMEYER, H. E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c379t-433bb6c3987777d1674c15aa95a2570d3e7718f46d1182c70a264656e22a74c33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Ageing, cell death</topic><topic>Animals</topic><topic>Anti-oncogenes</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Calcium-Calmodulin-Dependent Protein Kinases - antagonists & inhibitors</topic><topic>Calcium-Calmodulin-Dependent Protein Kinases - metabolism</topic><topic>Cell Line</topic><topic>Cell physiology</topic><topic>Cell Survival</topic><topic>Cytokines</topic><topic>DNA-Binding Proteins - antagonists & inhibitors</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Enzyme Activation</topic><topic>Enzyme inhibitors</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Flavonoids - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genotype</topic><topic>Granulocyte-Macrophage Colony-Stimulating Factor - metabolism</topic><topic>Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Janus Kinase 2</topic><topic>Kinases</topic><topic>MAP kinase</topic><topic>Mice</topic><topic>Milk Proteins</topic><topic>Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3</topic><topic>Mitogen-Activated Protein Kinases</topic><topic>Molecular and cellular biology</topic><topic>p53 Protein</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Promoter Regions, Genetic</topic><topic>Protein Conformation</topic><topic>Protein kinase</topic><topic>Protein kinase C</topic><topic>Protein-Tyrosine Kinases - antagonists & inhibitors</topic><topic>Protein-Tyrosine Kinases - metabolism</topic><topic>Proto-Oncogene Proteins</topic><topic>Signal transduction</topic><topic>STAT5 Transcription Factor</topic><topic>Thrombopoietin</topic><topic>Thrombopoietin - pharmacology</topic><topic>Time Factors</topic><topic>Trans-Activators - antagonists & inhibitors</topic><topic>Trans-Activators - metabolism</topic><topic>Tumor Suppressor Protein p53 - chemistry</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>RITCHIE, A</creatorcontrib><creatorcontrib>BRAUN, S. 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E</au><au>HE, J</au><au>BROXMEYER, H. E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thrombopoietin-induced conformational change in p53 lies downstream of the p44/p42 mitogen activated protein kinase cascade in the human growth factor-dependent cell line M07e</atitle><jtitle>Oncogene</jtitle><addtitle>Oncogene</addtitle><date>1999-02-18</date><risdate>1999</risdate><volume>18</volume><issue>7</issue><spage>1465</spage><epage>1477</epage><pages>1465-1477</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><abstract>Thrombopoietin is a cytokine with potent megakaryocytopoietic and thrombopoietic activities in vivo. Wild-type p53 is a conformationally flexible, anti-oncogenic transcription factor that plays a principal role in mediating growth factor withdrawal-induced apoptosis in factor-dependent hematopoietic cells. We recently reported that Tpo induces a conformational change in and functional inactivation of p53, coincident with its anti-apoptotic effects, in the human factor-dependent cell line M07e. In an effort to identify potential signaling cascades through which Tpo illicits these effects on p53, we report here that treating M07e cells with MAPK kinase inhibitor PD98059 dramatically suppressed Tpo-induced conformational change in p53 as well as Tpo-enhanced viability in M07e cells in a p53-dependent manner. Furthermore, the expression of constitutively active Raf1 in M07e cells induced conformational change in p53 independent of Tpo stimulation. Inhibition of the JAK/STAT pathway revealed that JAK/STAT signaling plays an insignificant role in conformational modulation of p53 and apoptosis suppression. Inhibition of phosphatidylinositol-3 kinase did not have a significant effect on p53 conformation but did have a weak but significant effect on Tpo-enhanced viability. Cytokine-induced activation of the MAPK pathway and the subsequent functional neutralization of p53, may be an event by which apoptosis is commonly suppressed in hematopoiesis.</abstract><cop>Basingstoke</cop><pub>Nature Publishing</pub><pmid>10050883</pmid><doi>10.1038/sj.onc.1202439</doi><tpages>13</tpages></addata></record> |
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| ispartof | Oncogene, 1999-02, Vol.18 (7), p.1465-1477 |
| issn | 0950-9232 1476-5594 |
| language | eng |
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| subjects | 1-Phosphatidylinositol 3-kinase Ageing, cell death Animals Anti-oncogenes Apoptosis Biological and medical sciences Calcium-Calmodulin-Dependent Protein Kinases - antagonists & inhibitors Calcium-Calmodulin-Dependent Protein Kinases - metabolism Cell Line Cell physiology Cell Survival Cytokines DNA-Binding Proteins - antagonists & inhibitors DNA-Binding Proteins - metabolism Enzyme Activation Enzyme inhibitors Enzyme Inhibitors - pharmacology Flavonoids - pharmacology Fundamental and applied biological sciences. Psychology Genotype Granulocyte-Macrophage Colony-Stimulating Factor - metabolism Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology Growth factors Humans Janus Kinase 2 Kinases MAP kinase Mice Milk Proteins Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases Molecular and cellular biology p53 Protein Phosphatidylinositol 3-Kinases - metabolism Promoter Regions, Genetic Protein Conformation Protein kinase Protein kinase C Protein-Tyrosine Kinases - antagonists & inhibitors Protein-Tyrosine Kinases - metabolism Proto-Oncogene Proteins Signal transduction STAT5 Transcription Factor Thrombopoietin Thrombopoietin - pharmacology Time Factors Trans-Activators - antagonists & inhibitors Trans-Activators - metabolism Tumor Suppressor Protein p53 - chemistry Tumor Suppressor Protein p53 - genetics Up-Regulation |
| title | Thrombopoietin-induced conformational change in p53 lies downstream of the p44/p42 mitogen activated protein kinase cascade in the human growth factor-dependent cell line M07e |
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