Caspase-3-mediated cleavage of PICOT in apoptosis.
Identifieur interne : 000780 ( Main/Exploration ); précédent : 000779; suivant : 000781Caspase-3-mediated cleavage of PICOT in apoptosis.
Auteurs : Nuri Yun [Corée du Sud] ; Chiho Kim ; Hyeseon Cha ; Woo Jin Park ; Hirohiko Shibayama ; Il-Seon Park ; Young J. OhSource :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2013.
Descripteurs français
- KwdFr :
- MESH :
- métabolisme : Caspase-3, Protéines de transport.
- Animaux, Apoptose, Cellules HEK293, Humains, Lignée cellulaire tumorale, Souris.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Carrier Proteins, Caspase 3.
- Animals, Apoptosis, Cell Line, Tumor, HEK293 Cells, Humans, Mice.
Abstract
Mammalian protein kinase C-interacting cousin of thioredoxin (PICOT) is a multi-domain mono-thiol glutaredoxin that is involved in several signal transduction pathways and is necessary for cell growth and metastasis. Here, we demonstrate that PICOT is a cleavage substrate of the apoptosis-related protein caspase-3. In vitro cleavage assays indicated that PICOT was specifically cleaved by caspase-3. Similarly, endogenous PICOT was cleaved in cell death responses induced by staurosporine and etoposide. These phenomena were blocked in the presence of a pan-caspase inhibitor. Using site-directed mutagenesis, we identified two putative caspase-3 cleavage sequences in PICOT, DRLD(101)/G and EELD(226)/T. Interestingly, overexpression of either PICOT wild type or the D101A/D226A double point mutant accelerated etoposide-induced activation of caspase-3 whereas siRNA-mediated knockdown of PICOT blocked this phenomenon. Our data raise the possibility that the pro-apoptotic role of PICOT is actively regulated via caspase-3-mediated cleavage.
DOI: 10.1016/j.bbrc.2013.02.017
PubMed: 23415866
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Oh</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="RBID">pubmed:23415866</idno><idno type="pmid">23415866</idno><idno type="doi">10.1016/j.bbrc.2013.02.017</idno><idno type="wicri:Area/Main/Corpus">000761</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000761</idno><idno type="wicri:Area/Main/Curation">000761</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000761</idno><idno type="wicri:Area/Main/Exploration">000761</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Caspase-3-mediated cleavage of PICOT in apoptosis.</title><author><name sortKey="Yun, Nuri" sort="Yun, Nuri" uniqKey="Yun N" first="Nuri" last="Yun">Nuri Yun</name><affiliation wicri:level="1"><nlm:affiliation>Department of Systems Biology, Yonsei University College of Life Science and Biotechnology, Seoul 120-749, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Systems Biology, Yonsei University College of Life Science and Biotechnology, Seoul 120-749</wicri:regionArea><placeName><settlement type="city">Séoul</settlement><region type="capital">Région capitale de Séoul</region></placeName></affiliation></author><author><name sortKey="Kim, Chiho" sort="Kim, Chiho" uniqKey="Kim C" first="Chiho" last="Kim">Chiho Kim</name></author><author><name sortKey="Cha, Hyeseon" sort="Cha, Hyeseon" uniqKey="Cha H" first="Hyeseon" last="Cha">Hyeseon Cha</name></author><author><name sortKey="Park, Woo Jin" sort="Park, Woo Jin" uniqKey="Park W" first="Woo Jin" last="Park">Woo Jin Park</name></author><author><name sortKey="Shibayama, Hirohiko" sort="Shibayama, Hirohiko" uniqKey="Shibayama H" first="Hirohiko" last="Shibayama">Hirohiko Shibayama</name></author><author><name sortKey="Park, Il Seon" sort="Park, Il Seon" uniqKey="Park I" first="Il-Seon" last="Park">Il-Seon Park</name></author><author><name sortKey="Oh, Young J" sort="Oh, Young J" uniqKey="Oh Y" first="Young J" last="Oh">Young J. Oh</name></author></analytic><series><title level="j">Biochemical and biophysical research communications</title><idno type="eISSN">1090-2104</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Apoptosis (MeSH)</term><term>Carrier Proteins (metabolism)</term><term>Caspase 3 (metabolism)</term><term>Cell Line, Tumor (MeSH)</term><term>HEK293 Cells (MeSH)</term><term>Humans (MeSH)</term><term>Mice (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Apoptose (MeSH)</term><term>Caspase-3 (métabolisme)</term><term>Cellules HEK293 (MeSH)</term><term>Humains (MeSH)</term><term>Lignée cellulaire tumorale (MeSH)</term><term>Protéines de transport (métabolisme)</term><term>Souris (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Carrier Proteins</term><term>Caspase 3</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspase-3</term><term>Protéines de transport</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Cell Line, Tumor</term><term>HEK293 Cells</term><term>Humans</term><term>Mice</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Cellules HEK293</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mammalian protein kinase C-interacting cousin of thioredoxin (PICOT) is a multi-domain mono-thiol glutaredoxin that is involved in several signal transduction pathways and is necessary for cell growth and metastasis. Here, we demonstrate that PICOT is a cleavage substrate of the apoptosis-related protein caspase-3. In vitro cleavage assays indicated that PICOT was specifically cleaved by caspase-3. Similarly, endogenous PICOT was cleaved in cell death responses induced by staurosporine and etoposide. These phenomena were blocked in the presence of a pan-caspase inhibitor. Using site-directed mutagenesis, we identified two putative caspase-3 cleavage sequences in PICOT, DRLD(101)/G and EELD(226)/T. Interestingly, overexpression of either PICOT wild type or the D101A/D226A double point mutant accelerated etoposide-induced activation of caspase-3 whereas siRNA-mediated knockdown of PICOT blocked this phenomenon. Our data raise the possibility that the pro-apoptotic role of PICOT is actively regulated via caspase-3-mediated cleavage.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23415866</PMID><DateCompleted><Year>2013</Year><Month>09</Month><Day>09</Day></DateCompleted><DateRevised><Year>2013</Year><Month>03</Month><Day>18</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2104</ISSN><JournalIssue CitedMedium="Internet"><Volume>432</Volume><Issue>3</Issue><PubDate><Year>2013</Year><Month>Mar</Month><Day>15</Day></PubDate></JournalIssue><Title>Biochemical and biophysical research communications</Title><ISOAbbreviation>Biochem Biophys Res Commun</ISOAbbreviation></Journal><ArticleTitle>Caspase-3-mediated cleavage of PICOT in apoptosis.</ArticleTitle><Pagination><MedlinePgn>533-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbrc.2013.02.017</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0006-291X(13)00262-3</ELocationID><Abstract><AbstractText>Mammalian protein kinase C-interacting cousin of thioredoxin (PICOT) is a multi-domain mono-thiol glutaredoxin that is involved in several signal transduction pathways and is necessary for cell growth and metastasis. Here, we demonstrate that PICOT is a cleavage substrate of the apoptosis-related protein caspase-3. In vitro cleavage assays indicated that PICOT was specifically cleaved by caspase-3. Similarly, endogenous PICOT was cleaved in cell death responses induced by staurosporine and etoposide. These phenomena were blocked in the presence of a pan-caspase inhibitor. Using site-directed mutagenesis, we identified two putative caspase-3 cleavage sequences in PICOT, DRLD(101)/G and EELD(226)/T. Interestingly, overexpression of either PICOT wild type or the D101A/D226A double point mutant accelerated etoposide-induced activation of caspase-3 whereas siRNA-mediated knockdown of PICOT blocked this phenomenon. Our data raise the possibility that the pro-apoptotic role of PICOT is actively regulated via caspase-3-mediated cleavage.</AbstractText><CopyrightInformation>Copyright © 2013 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yun</LastName><ForeName>Nuri</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Systems Biology, Yonsei University College of Life Science and Biotechnology, Seoul 120-749, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Chiho</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Cha</LastName><ForeName>Hyeseon</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Woo Jin</ForeName><Initials>WJ</Initials></Author><Author ValidYN="Y"><LastName>Shibayama</LastName><ForeName>Hirohiko</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Il-Seon</ForeName><Initials>IS</Initials></Author><Author ValidYN="Y"><LastName>Oh</LastName><ForeName>Young J</ForeName><Initials>YJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>02</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Biochem Biophys Res Commun</MedlineTA><NlmUniqueID>0372516</NlmUniqueID><ISSNLinking>0006-291X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002352">Carrier Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C404105">GLRX3 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D053148">Caspase 3</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="Y">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002352" MajorTopicYN="N">Carrier Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053148" MajorTopicYN="N">Caspase 3</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D057809" MajorTopicYN="N">HEK293 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year><Month>02</Month><Day>01</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2013</Year><Month>02</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>2</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>2</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>9</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23415866</ArticleId><ArticleId IdType="pii">S0006-291X(13)00262-3</ArticleId><ArticleId IdType="doi">10.1016/j.bbrc.2013.02.017</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Corée du Sud</li></country><region><li>Région capitale de Séoul</li></region><settlement><li>Séoul</li></settlement></list><tree><noCountry><name sortKey="Cha, Hyeseon" sort="Cha, Hyeseon" uniqKey="Cha H" first="Hyeseon" last="Cha">Hyeseon Cha</name><name sortKey="Kim, Chiho" sort="Kim, Chiho" uniqKey="Kim C" first="Chiho" last="Kim">Chiho Kim</name><name sortKey="Oh, Young J" sort="Oh, Young J" uniqKey="Oh Y" first="Young J" last="Oh">Young J. Oh</name><name sortKey="Park, Il Seon" sort="Park, Il Seon" uniqKey="Park I" first="Il-Seon" last="Park">Il-Seon Park</name><name sortKey="Park, Woo Jin" sort="Park, Woo Jin" uniqKey="Park W" first="Woo Jin" last="Park">Woo Jin Park</name><name sortKey="Shibayama, Hirohiko" sort="Shibayama, Hirohiko" uniqKey="Shibayama H" first="Hirohiko" last="Shibayama">Hirohiko Shibayama</name></noCountry><country name="Corée du Sud"><region name="Région capitale de Séoul"><name sortKey="Yun, Nuri" sort="Yun, Nuri" uniqKey="Yun N" first="Nuri" last="Yun">Nuri Yun</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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