Inhibition of FoxO1 acetylation by INHAT subunit SET/TAF-Iβ induces p21 transcription

•SET/TAF-Iβ inhibits FoxO1 acetylation.•SET/TAF-Iβ interacts with FoxO1 in INHAT domain dependent manner.•Recruitment of FoxO1 on p21 promoter is increased by SET/TAF-Iβ.•SET/TAF-Iβ induces p21 transcription and apoptosis under oxidative stress. Post-translational modification of forkhead family tra...

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Veröffentlicht in:FEBS letters 2014-08, Vol.588 (17), p.2867-2873
Hauptverfasser: Chae, Yun-Cheol, Kim, Kee-Beom, Kang, Joo-Young, Kim, Se-Ryeon, Jung, Hyeon-Soo, Seo, Sang-Beom
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container_end_page 2873
container_issue 17
container_start_page 2867
container_title FEBS letters
container_volume 588
creator Chae, Yun-Cheol
Kim, Kee-Beom
Kang, Joo-Young
Kim, Se-Ryeon
Jung, Hyeon-Soo
Seo, Sang-Beom
description •SET/TAF-Iβ inhibits FoxO1 acetylation.•SET/TAF-Iβ interacts with FoxO1 in INHAT domain dependent manner.•Recruitment of FoxO1 on p21 promoter is increased by SET/TAF-Iβ.•SET/TAF-Iβ induces p21 transcription and apoptosis under oxidative stress. Post-translational modification of forkhead family transcription factor, FoxO1, is an important regulatory mode for its diverse activities. FoxO1 is acetylated by HAT coactivators and its transcriptional activity is decreased via reduced DNA binding affinity. Here, we report that SET/TAF-Iβ inhibited p300-mediated FoxO1 acetylation in an INHAT domain-dependent manner. SET/TAF-Iβ interacted with FoxO1 and activated transcription of FoxO1 target gene, p21. Moreover, SET/TAF-Iβ inhibited acetylation of FoxO1 and increased p21 transcription induced by oxidative stress. Our results suggest that SET/TAF-Iβ inhibits FoxO1 acetylation and activates its transcriptional activity toward p21. FoxO1physically interacts with SET/TAF-Iβ by pull down (1, 2) FoxO1physically interacts with SET/TAF-Iβ by anti tag coimmunoprecipitation (View interaction) SET/TAF-Iβphysically interacts with FoxO1 by anti bait coip (1, 2)
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Post-translational modification of forkhead family transcription factor, FoxO1, is an important regulatory mode for its diverse activities. FoxO1 is acetylated by HAT coactivators and its transcriptional activity is decreased via reduced DNA binding affinity. Here, we report that SET/TAF-Iβ inhibited p300-mediated FoxO1 acetylation in an INHAT domain-dependent manner. SET/TAF-Iβ interacted with FoxO1 and activated transcription of FoxO1 target gene, p21. Moreover, SET/TAF-Iβ inhibited acetylation of FoxO1 and increased p21 transcription induced by oxidative stress. Our results suggest that SET/TAF-Iβ inhibits FoxO1 acetylation and activates its transcriptional activity toward p21. 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Post-translational modification of forkhead family transcription factor, FoxO1, is an important regulatory mode for its diverse activities. FoxO1 is acetylated by HAT coactivators and its transcriptional activity is decreased via reduced DNA binding affinity. Here, we report that SET/TAF-Iβ inhibited p300-mediated FoxO1 acetylation in an INHAT domain-dependent manner. SET/TAF-Iβ interacted with FoxO1 and activated transcription of FoxO1 target gene, p21. Moreover, SET/TAF-Iβ inhibited acetylation of FoxO1 and increased p21 transcription induced by oxidative stress. Our results suggest that SET/TAF-Iβ inhibits FoxO1 acetylation and activates its transcriptional activity toward p21. FoxO1physically interacts with SET/TAF-Iβ by pull down (1, 2) FoxO1physically interacts with SET/TAF-Iβ by anti tag coimmunoprecipitation (View interaction) SET/TAF-Iβphysically interacts with FoxO1 by anti bait coip (1, 2)</description><subject>Acetylation</subject><subject>Apoptosis</subject><subject>binding capacity</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - genetics</subject><subject>DNA</subject><subject>Forkhead Box Protein O1</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>FoxO1</subject><subject>Gene Expression Regulation</subject><subject>genes</subject><subject>HCT116 Cells</subject><subject>HEK293 Cells</subject><subject>Histone Chaperones - metabolism</subject><subject>Humans</subject><subject>Oxidative Stress</subject><subject>p21</subject><subject>post-translational modification</subject><subject>Protein Subunits - metabolism</subject><subject>SET/TAF-Iβ</subject><subject>Transcription</subject><subject>transcription (genetics)</subject><subject>transcription factors</subject><subject>Transcription Factors - metabolism</subject><subject>Transcription, Genetic</subject><issn>0014-5793</issn><issn>1873-3468</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc2O0zAUhS0EYsrAI4C8ZJOM_-usUBm1tNKIWUxBs7Ns50a4SpNiJ0BfiwfhmXBoYVsWtq_tc4599SH0mpKSEqpudmUDLrUwlIxQURJVEsmfoBnVc15wofRTNCP5ppDzil-hFyntSN5rWj1HV0xUmucxQ5833ZfgwhD6DvcNXvU_7im2HoZja_8cuiPefFwvtjiNbuzCgB-W25vtYlVsfv3EoatHDwkfGMVDtF3yMRwm20v0rLFtglfn9Rp9Wi23t-vi7v7D5nZxV3hRqceimddWM50n8EBBWqsEq4B74RsnaC6ZA-eZoDK3oTUH54iqa0Iq5bnj_Bq9PeUeYv91hDSYfUge2tZ20I_JsNwzoxVR5KKUKi4J5ZJVl6VSCqHYXIsslSepj31KERpziGFv49FQYiZQZmfOoMwEyhBlMqjse3N-YnR7qP-5_pLJgvVJ8D20cPy_VLNavmcPE_UJOhWESKoec9S7UxRkEt8CRJN8gM5DHSL4wdR9uPDb30qwuyU</recordid><startdate>20140825</startdate><enddate>20140825</enddate><creator>Chae, Yun-Cheol</creator><creator>Kim, Kee-Beom</creator><creator>Kang, Joo-Young</creator><creator>Kim, Se-Ryeon</creator><creator>Jung, Hyeon-Soo</creator><creator>Seo, Sang-Beom</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</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>7X8</scope><scope>7TO</scope><scope>H94</scope><scope>7S9</scope><scope>L.6</scope></search><sort><creationdate>20140825</creationdate><title>Inhibition of FoxO1 acetylation by INHAT subunit SET/TAF-Iβ induces p21 transcription</title><author>Chae, Yun-Cheol ; Kim, Kee-Beom ; Kang, Joo-Young ; Kim, Se-Ryeon ; Jung, Hyeon-Soo ; Seo, Sang-Beom</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c496X-f7da828da8ece1e5aa6429e3c4cfb4129e2bebc2415579883ebb06dd0096c3b33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Acetylation</topic><topic>Apoptosis</topic><topic>binding capacity</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - genetics</topic><topic>DNA</topic><topic>Forkhead Box Protein O1</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>FoxO1</topic><topic>Gene Expression Regulation</topic><topic>genes</topic><topic>HCT116 Cells</topic><topic>HEK293 Cells</topic><topic>Histone Chaperones - metabolism</topic><topic>Humans</topic><topic>Oxidative Stress</topic><topic>p21</topic><topic>post-translational modification</topic><topic>Protein Subunits - metabolism</topic><topic>SET/TAF-Iβ</topic><topic>Transcription</topic><topic>transcription (genetics)</topic><topic>transcription factors</topic><topic>Transcription Factors - metabolism</topic><topic>Transcription, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chae, Yun-Cheol</creatorcontrib><creatorcontrib>Kim, Kee-Beom</creatorcontrib><creatorcontrib>Kang, Joo-Young</creatorcontrib><creatorcontrib>Kim, Se-Ryeon</creatorcontrib><creatorcontrib>Jung, Hyeon-Soo</creatorcontrib><creatorcontrib>Seo, Sang-Beom</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>FEBS letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chae, Yun-Cheol</au><au>Kim, Kee-Beom</au><au>Kang, Joo-Young</au><au>Kim, Se-Ryeon</au><au>Jung, Hyeon-Soo</au><au>Seo, Sang-Beom</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of FoxO1 acetylation by INHAT subunit SET/TAF-Iβ induces p21 transcription</atitle><jtitle>FEBS letters</jtitle><addtitle>FEBS Lett</addtitle><date>2014-08-25</date><risdate>2014</risdate><volume>588</volume><issue>17</issue><spage>2867</spage><epage>2873</epage><pages>2867-2873</pages><issn>0014-5793</issn><eissn>1873-3468</eissn><abstract>•SET/TAF-Iβ inhibits FoxO1 acetylation.•SET/TAF-Iβ interacts with FoxO1 in INHAT domain dependent manner.•Recruitment of FoxO1 on p21 promoter is increased by SET/TAF-Iβ.•SET/TAF-Iβ induces p21 transcription and apoptosis under oxidative stress. Post-translational modification of forkhead family transcription factor, FoxO1, is an important regulatory mode for its diverse activities. FoxO1 is acetylated by HAT coactivators and its transcriptional activity is decreased via reduced DNA binding affinity. Here, we report that SET/TAF-Iβ inhibited p300-mediated FoxO1 acetylation in an INHAT domain-dependent manner. SET/TAF-Iβ interacted with FoxO1 and activated transcription of FoxO1 target gene, p21. Moreover, SET/TAF-Iβ inhibited acetylation of FoxO1 and increased p21 transcription induced by oxidative stress. Our results suggest that SET/TAF-Iβ inhibits FoxO1 acetylation and activates its transcriptional activity toward p21. FoxO1physically interacts with SET/TAF-Iβ by pull down (1, 2) FoxO1physically interacts with SET/TAF-Iβ by anti tag coimmunoprecipitation (View interaction) SET/TAF-Iβphysically interacts with FoxO1 by anti bait coip (1, 2)</abstract><cop>England</cop><pub>Elsevier B.V</pub><pmid>24983498</pmid><doi>10.1016/j.febslet.2014.06.053</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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source Wiley Free Content; MEDLINE; Wiley Online Library Journals Frontfile Complete; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection
subjects Acetylation
Apoptosis
binding capacity
Cyclin-Dependent Kinase Inhibitor p21 - genetics
DNA
Forkhead Box Protein O1
Forkhead Transcription Factors - metabolism
FoxO1
Gene Expression Regulation
genes
HCT116 Cells
HEK293 Cells
Histone Chaperones - metabolism
Humans
Oxidative Stress
p21
post-translational modification
Protein Subunits - metabolism
SET/TAF-Iβ
Transcription
transcription (genetics)
transcription factors
Transcription Factors - metabolism
Transcription, Genetic
title Inhibition of FoxO1 acetylation by INHAT subunit SET/TAF-Iβ induces p21 transcription
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