| Differential cleavage of Mst1 by caspase-7/-3 is responsible for TRAIL-induced activation of the MAPK superfamily. | |
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MedLine Citation:
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PMID: 18276109 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown to induce apoptosis through caspase activation in a number of cancer cell lines while displaying minimal or no toxicity on normal cells, suggesting that this protein may hold potential for development as a new cancer therapeutic agent. Moreover, TRAIL can activate mitogen-activated protein kinases (MAPKs) in addition to caspases. However, it has not been clearly understood how MAPKs are activated by TRAIL and the biological significance of their activation. Here we show that TRAIL-induced MAPKs activation is dependent on caspase activation and that mammalian sterile 20-like kinase 1 (Mst1) functions as a mediator between caspase activation and MAPKs activation. Activation of MAPKs (JNK, p38, ERK) is differentially regulated by cleavage size (40 kDa and 36 kDa) of Mst1, which is controlled by caspase-7 and -3. |
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Authors:
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Jae J Song; Yong J Lee |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. Date: 2008-01-11 |
Journal Detail:
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Title: Cellular signalling Volume: 20 ISSN: 0898-6568 ISO Abbreviation: Cell. Signal. Publication Date: 2008 May |
Date Detail:
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Created Date: 2008-03-07 Completed Date: 2008-05-23 Revised Date: 2013-02-13 |
Medline Journal Info:
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Nlm Unique ID: 8904683 Medline TA: Cell Signal Country: England |
Other Details:
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Languages: eng Pagination: 892-906 Citation Subset: IM |
Affiliation:
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Department of Surgery and Pharmacology, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Base Sequence Caspase 3 / genetics, metabolism* Caspase 7 / genetics, metabolism* Cell Line, Tumor DNA Primers / genetics Female Hepatocyte Growth Factor / antagonists & inhibitors, genetics, metabolism* Humans MAP Kinase Signaling System / drug effects*, physiology Male Mutagenesis, Site-Directed Proto-Oncogene Proteins / antagonists & inhibitors, genetics, metabolism* RNA, Small Interfering / genetics Reactive Oxygen Species / metabolism Recombinant Proteins / genetics, metabolism, pharmacology Sequence Deletion TNF-Related Apoptosis-Inducing Ligand / genetics, metabolism, pharmacology* Transfection |
| Grant Support | |
ID/Acronym/Agency:
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CA121395/CA/NCI NIH HHS; CA95191/CA/NCI NIH HHS; CA96989/CA/NCI NIH HHS; R01 CA095191/CA/NCI NIH HHS; R01 CA095191-01A2/CA/NCI NIH HHS; R01 CA096989/CA/NCI NIH HHS; R01 CA096989-01A2/CA/NCI NIH HHS; R03 CA121395/CA/NCI NIH HHS; R03 CA121395-01/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/DNA Primers; 0/Proto-Oncogene Proteins; 0/RNA, Small Interfering; 0/Reactive Oxygen Species; 0/Recombinant Proteins; 0/TNF-Related Apoptosis-Inducing Ligand; 0/TNFSF10 protein, human; 0/macrophage stimulating protein; 67256-21-7/Hepatocyte Growth Factor; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/CASP7 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 7 |
| Comments/Corrections | |
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