PI3K activates negative and positive signals to regulate TRB3 expression in hepatic cells
TRB3 is a pseudokinase whose expression is regulated during stress response and changing of nutrient status. TRB3 negatively regulates Akt activation and noticeably, TRB3 expression is induced by insulin. Here, we sought to determine the dynamic relationship between TRB3 expression and Akt activatio...
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| Veröffentlicht in: | Experimental cell research 2008-04, Vol.314 (7), p.1566-1574 |
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| creator | Ding, Jixin Kato, Satomi Du, Keyong |
| description | TRB3 is a pseudokinase whose expression is regulated during stress response and changing of nutrient status. TRB3 negatively regulates Akt activation and noticeably, TRB3 expression is induced by insulin. Here, we sought to determine the dynamic relationship between TRB3 expression and Akt activation. We find that insulin induces TRB3 expression in cell type dependent manner such that in hepatic cells and adipocytes but not Beta cells and muscle cells. In Fao hepatoma cells, induction of TRB3 expression by insulin restrains Akt activation and renders Akt refractory to further activation. In addition, we have also analyzed the roles of PI3K and its downstream kinases Akt and atypical PKC in TRB3 expression. Induction of TRB3 expression by insulin requires PI3K. However, inactivation of Akt enhances TRB3 expression whereas inhibition of PKCζ expression impairs TRB3 expression induced by insulin. Our data demonstrated that PI3K conveys both negative and positive signals to TRB3 expression. We suggest that insulin-induced TRB3 expression functions as an indicator how multiple insulin-induced signal transduction pathways are balanced. |
| doi_str_mv | 10.1016/j.yexcr.2008.01.026 |
| format | Article |
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TRB3 negatively regulates Akt activation and noticeably, TRB3 expression is induced by insulin. Here, we sought to determine the dynamic relationship between TRB3 expression and Akt activation. We find that insulin induces TRB3 expression in cell type dependent manner such that in hepatic cells and adipocytes but not Beta cells and muscle cells. In Fao hepatoma cells, induction of TRB3 expression by insulin restrains Akt activation and renders Akt refractory to further activation. In addition, we have also analyzed the roles of PI3K and its downstream kinases Akt and atypical PKC in TRB3 expression. Induction of TRB3 expression by insulin requires PI3K. However, inactivation of Akt enhances TRB3 expression whereas inhibition of PKCζ expression impairs TRB3 expression induced by insulin. Our data demonstrated that PI3K conveys both negative and positive signals to TRB3 expression. We suggest that insulin-induced TRB3 expression functions as an indicator how multiple insulin-induced signal transduction pathways are balanced.</description><identifier>ISSN: 0014-4827</identifier><identifier>EISSN: 1090-2422</identifier><identifier>DOI: 10.1016/j.yexcr.2008.01.026</identifier><identifier>PMID: 18316073</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>3T3-L1 Cells ; Akt atypical PKC ; Animals ; Cell Cycle Proteins - genetics ; Cell Cycle Proteins - metabolism ; Cellular biology ; Enzyme Activation - drug effects ; Hepatocytes - drug effects ; Hepatocytes - enzymology ; Hepatocytes - metabolism ; Humans ; Insulin ; Insulin - pharmacology ; Insulin gene expression ; Kinases ; Liver ; Mice ; Organ Specificity - drug effects ; P13K ; Phosphatidylinositol 3-Kinases - metabolism ; Promoter Regions, Genetic - genetics ; Protein Kinase C - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Signal transduction ; Signal Transduction - drug effects ; TRB3</subject><ispartof>Experimental cell research, 2008-04, Vol.314 (7), p.1566-1574</ispartof><rights>2008 Elsevier Inc.</rights><rights>Copyright © 2008 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c450t-77eebe69d204b68b9075bd205dcd988fbcaa59fc08b924745ae3af11a5c4ab53</citedby><cites>FETCH-LOGICAL-c450t-77eebe69d204b68b9075bd205dcd988fbcaa59fc08b924745ae3af11a5c4ab53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S001448270800075X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18316073$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ding, Jixin</creatorcontrib><creatorcontrib>Kato, Satomi</creatorcontrib><creatorcontrib>Du, Keyong</creatorcontrib><title>PI3K activates negative and positive signals to regulate TRB3 expression in hepatic cells</title><title>Experimental cell research</title><addtitle>Exp Cell Res</addtitle><description>TRB3 is a pseudokinase whose expression is regulated during stress response and changing of nutrient status. TRB3 negatively regulates Akt activation and noticeably, TRB3 expression is induced by insulin. Here, we sought to determine the dynamic relationship between TRB3 expression and Akt activation. We find that insulin induces TRB3 expression in cell type dependent manner such that in hepatic cells and adipocytes but not Beta cells and muscle cells. In Fao hepatoma cells, induction of TRB3 expression by insulin restrains Akt activation and renders Akt refractory to further activation. In addition, we have also analyzed the roles of PI3K and its downstream kinases Akt and atypical PKC in TRB3 expression. Induction of TRB3 expression by insulin requires PI3K. However, inactivation of Akt enhances TRB3 expression whereas inhibition of PKCζ expression impairs TRB3 expression induced by insulin. Our data demonstrated that PI3K conveys both negative and positive signals to TRB3 expression. 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Kato, Satomi ; Du, Keyong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c450t-77eebe69d204b68b9075bd205dcd988fbcaa59fc08b924745ae3af11a5c4ab53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>3T3-L1 Cells</topic><topic>Akt atypical PKC</topic><topic>Animals</topic><topic>Cell Cycle Proteins - genetics</topic><topic>Cell Cycle Proteins - metabolism</topic><topic>Cellular biology</topic><topic>Enzyme Activation - drug effects</topic><topic>Hepatocytes - drug effects</topic><topic>Hepatocytes - enzymology</topic><topic>Hepatocytes - metabolism</topic><topic>Humans</topic><topic>Insulin</topic><topic>Insulin - pharmacology</topic><topic>Insulin gene expression</topic><topic>Kinases</topic><topic>Liver</topic><topic>Mice</topic><topic>Organ Specificity - drug effects</topic><topic>P13K</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Protein Kinase C - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>TRB3</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ding, Jixin</creatorcontrib><creatorcontrib>Kato, Satomi</creatorcontrib><creatorcontrib>Du, Keyong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental cell research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ding, Jixin</au><au>Kato, Satomi</au><au>Du, Keyong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PI3K activates negative and positive signals to regulate TRB3 expression in hepatic cells</atitle><jtitle>Experimental cell research</jtitle><addtitle>Exp Cell Res</addtitle><date>2008-04-15</date><risdate>2008</risdate><volume>314</volume><issue>7</issue><spage>1566</spage><epage>1574</epage><pages>1566-1574</pages><issn>0014-4827</issn><eissn>1090-2422</eissn><abstract>TRB3 is a pseudokinase whose expression is regulated during stress response and changing of nutrient status. TRB3 negatively regulates Akt activation and noticeably, TRB3 expression is induced by insulin. Here, we sought to determine the dynamic relationship between TRB3 expression and Akt activation. We find that insulin induces TRB3 expression in cell type dependent manner such that in hepatic cells and adipocytes but not Beta cells and muscle cells. In Fao hepatoma cells, induction of TRB3 expression by insulin restrains Akt activation and renders Akt refractory to further activation. In addition, we have also analyzed the roles of PI3K and its downstream kinases Akt and atypical PKC in TRB3 expression. Induction of TRB3 expression by insulin requires PI3K. However, inactivation of Akt enhances TRB3 expression whereas inhibition of PKCζ expression impairs TRB3 expression induced by insulin. Our data demonstrated that PI3K conveys both negative and positive signals to TRB3 expression. 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| subjects | 3T3-L1 Cells Akt atypical PKC Animals Cell Cycle Proteins - genetics Cell Cycle Proteins - metabolism Cellular biology Enzyme Activation - drug effects Hepatocytes - drug effects Hepatocytes - enzymology Hepatocytes - metabolism Humans Insulin Insulin - pharmacology Insulin gene expression Kinases Liver Mice Organ Specificity - drug effects P13K Phosphatidylinositol 3-Kinases - metabolism Promoter Regions, Genetic - genetics Protein Kinase C - metabolism Proto-Oncogene Proteins c-akt - metabolism Signal transduction Signal Transduction - drug effects TRB3 |
| title | PI3K activates negative and positive signals to regulate TRB3 expression in hepatic cells |
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