Correlation between TGF‐β1 expression and proteomic profiling induced by severe acute respiratory syndrome coronavirus papain‐like protease
Identifieur interne : 001F32 ( Main/Merge ); précédent : 001F31; suivant : 001F33Correlation between TGF‐β1 expression and proteomic profiling induced by severe acute respiratory syndrome coronavirus papain‐like protease
Auteurs : Shih-Wen Li [Taïwan] ; Tsuey-Ching Yang [Taïwan] ; Lei Wan [Taïwan] ; Ying-Ju Lin [Taïwan] ; Fuu-Jen Tsai [Taïwan] ; Chien-Chen Lai [Taïwan] ; Cheng-Wen Lin [Taïwan]Source :
- PROTEOMICS [ 1615-9853 ] ; 2012-11.
Abstract
Severe acute respiratory syndrome (SARS) coronavirus (SARS‐CoV) papain‐like protease (PLpro), a deubiquitinating enzyme, demonstrates inactivation of interferon (IFN) regulatory factor 3 and NF‐κB, reduction of IFN induction, and suppression of type I IFN signaling pathway. This study investigates cytokine expression and proteomic change induced by SARS‐CoV PLpro in human promonocyte cells. PLpro significantly increased TGF‐β1 mRNA expression (greater than fourfold) and protein production (greater than threefold). Proteomic analysis, Western blot, and quantitative real‐time PCR assays indicated PLpro upregulating TGF‐β1‐associated genes: HSP27, protein disulfide isomerase A3 precursor, glial fibrillary acidic protein, vimentin, retinal dehydrogenase 2, and glutathione transferase omega‐1. PLpro‐activated ubiquitin proteasome pathway via upregulation of ubiquitin‐conjugating enzyme E2–25k and proteasome subunit alpha type 5. Proteasome inhibitor MG‐132 significantly reduced expression of TGF‐β1 and vimentin. PLpro upregulated HSP27, linking with activation of p38 MAPK and ERK1/2 signaling. Treatment with SB203580 and U0126 reduced PLpro‐induced expression of TGF‐β1, vimentin, and type I collagen. Results point to SARS‐CoV PLpro triggering TGF‐β1 production via ubiquitin proteasome, p38 MAPK, and ERK1/2‐mediated signaling.
Url:
- https://api.istex.fr/ark:/67375/WNG-544ZDXNC-K/fulltext.pdf
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7168038
DOI: 10.1002/pmic.201200225
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Lei" sort="Wan, Lei" uniqKey="Wan L" first="Lei" last="Wan">Lei Wan</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Lin, Ying U" sort="Lin, Ying U" uniqKey="Lin Y" first="Ying-Ju" last="Lin">Ying-Ju Lin</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Tsai, Fuu En" sort="Tsai, Fuu En" uniqKey="Tsai F" first="Fuu-Jen" last="Tsai">Fuu-Jen Tsai</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medical Genetics and Medical Research, China Medical 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wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Clinical Virology Laboratory, Department of Laboratory Medicine, China Medical University Hospital, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Biotechnology, Asia University, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation><affiliation></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Taïwan</country></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">PROTEOMICS</title><title level="j" type="alt">PROTEOMICS</title><idno type="ISSN">1615-9853</idno><idno type="eISSN">1615-9861</idno><imprint><biblScope unit="vol">12</biblScope><biblScope unit="issue">21</biblScope><biblScope unit="page" from="3193">3193</biblScope><biblScope unit="page" to="3205">3205</biblScope><biblScope unit="page-count">13</biblScope><date type="published" when="2012-11">2012-11</date></imprint><idno type="ISSN">1615-9853</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1615-9853</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Severe acute respiratory syndrome (SARS) coronavirus (SARS‐CoV) papain‐like protease (PLpro), a deubiquitinating enzyme, demonstrates inactivation of interferon (IFN) regulatory factor 3 and NF‐κB, reduction of IFN induction, and suppression of type I IFN signaling pathway. This study investigates cytokine expression and proteomic change induced by SARS‐CoV PLpro in human promonocyte cells. PLpro significantly increased TGF‐β1 mRNA expression (greater than fourfold) and protein production (greater than threefold). Proteomic analysis, Western blot, and quantitative real‐time PCR assays indicated PLpro upregulating TGF‐β1‐associated genes: HSP27, protein disulfide isomerase A3 precursor, glial fibrillary acidic protein, vimentin, retinal dehydrogenase 2, and glutathione transferase omega‐1. PLpro‐activated ubiquitin proteasome pathway via upregulation of ubiquitin‐conjugating enzyme E2–25k and proteasome subunit alpha type 5. Proteasome inhibitor MG‐132 significantly reduced expression of TGF‐β1 and vimentin. PLpro upregulated HSP27, linking with activation of p38 MAPK and ERK1/2 signaling. Treatment with SB203580 and U0126 reduced PLpro‐induced expression of TGF‐β1, vimentin, and type I collagen. Results point to SARS‐CoV PLpro triggering TGF‐β1 production via ubiquitin proteasome, p38 MAPK, and ERK1/2‐mediated signaling.</div></front></TEI><double doi="10.1002/pmic.201200225"><ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Correlation between TGF‐β1 expression and proteomic profiling induced by severe acute respiratory syndrome coronavirus papain‐like protease</title><author><name sortKey="Li, Shih En" sort="Li, Shih En" uniqKey="Li S" first="Shih-Wen" last="Li">Shih-Wen Li</name></author><author><name sortKey="Yang, Tsuey Hing" sort="Yang, Tsuey Hing" uniqKey="Yang T" first="Tsuey-Ching" last="Yang">Tsuey-Ching Yang</name></author><author><name sortKey="Wan, Lei" sort="Wan, Lei" uniqKey="Wan L" first="Lei" last="Wan">Lei Wan</name></author><author><name sortKey="Lin, Ying U" sort="Lin, Ying U" uniqKey="Lin Y" first="Ying-Ju" last="Lin">Ying-Ju Lin</name></author><author><name sortKey="Tsai, Fuu En" sort="Tsai, Fuu En" uniqKey="Tsai F" first="Fuu-Jen" last="Tsai">Fuu-Jen Tsai</name></author><author><name sortKey="Lai, Chien Hen" sort="Lai, Chien Hen" uniqKey="Lai C" first="Chien-Chen" last="Lai">Chien-Chen Lai</name></author><author><name sortKey="Lin, Cheng En" sort="Lin, Cheng En" uniqKey="Lin C" first="Cheng-Wen" last="Lin">Cheng-Wen Lin</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:315E3998EFDD7D5375655F657609DE9A9755D6F9</idno><date when="2012" year="2012">2012</date><idno type="doi">10.1002/pmic.201200225</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-544ZDXNC-K/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000B39</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000B39</idno><idno type="wicri:Area/Istex/Curation">000B39</idno><idno type="wicri:Area/Istex/Checkpoint">000619</idno><idno type="wicri:explorRef" wicri:stream="Istex" 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sort="Yang, Tsuey Hing" uniqKey="Yang T" first="Tsuey-Ching" last="Yang">Tsuey-Ching Yang</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Biotechnology and Laboratory Science in Medicine, National Yang Ming University, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Wan, Lei" sort="Wan, Lei" uniqKey="Wan L" first="Lei" last="Wan">Lei Wan</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Lin, Ying U" sort="Lin, Ying U" uniqKey="Lin Y" first="Ying-Ju" last="Lin">Ying-Ju Lin</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Tsai, Fuu En" sort="Tsai, Fuu En" uniqKey="Tsai F" first="Fuu-Jen" last="Tsai">Fuu-Jen Tsai</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation></author><author><name sortKey="Lai, Chien Hen" sort="Lai, Chien Hen" uniqKey="Lai C" first="Chien-Chen" last="Lai">Chien-Chen Lai</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Institute of Molecular Biology, National Chung Hsing University, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medical Genetics and Medical Research, China Medical University Hospital, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation><affiliation></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Taïwan</country></affiliation></author><author><name sortKey="Lin, Cheng En" sort="Lin, Cheng En" uniqKey="Lin C" first="Cheng-Wen" last="Lin">Cheng-Wen Lin</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Clinical Virology Laboratory, Department of Laboratory Medicine, China Medical University Hospital, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Biotechnology, Asia University, Taichung</wicri:regionArea><wicri:noRegion>Taichung</wicri:noRegion></affiliation><affiliation></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Taïwan</country></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">PROTEOMICS</title><title level="j" type="alt">PROTEOMICS</title><idno type="ISSN">1615-9853</idno><idno type="eISSN">1615-9861</idno><imprint><biblScope unit="vol">12</biblScope><biblScope unit="issue">21</biblScope><biblScope unit="page" from="3193">3193</biblScope><biblScope unit="page" to="3205">3205</biblScope><biblScope unit="page-count">13</biblScope><date type="published" when="2012-11">2012-11</date></imprint><idno type="ISSN">1615-9853</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1615-9853</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Severe acute respiratory syndrome (SARS) coronavirus (SARS‐CoV) papain‐like protease (PLpro), a deubiquitinating enzyme, demonstrates inactivation of interferon (IFN) regulatory factor 3 and NF‐κB, reduction of IFN induction, and suppression of type I IFN signaling pathway. This study investigates cytokine expression and proteomic change induced by SARS‐CoV PLpro in human promonocyte cells. PLpro significantly increased TGF‐β1 mRNA expression (greater than fourfold) and protein production (greater than threefold). Proteomic analysis, Western blot, and quantitative real‐time PCR assays indicated PLpro upregulating TGF‐β1‐associated genes: HSP27, protein disulfide isomerase A3 precursor, glial fibrillary acidic protein, vimentin, retinal dehydrogenase 2, and glutathione transferase omega‐1. PLpro‐activated ubiquitin proteasome pathway via upregulation of ubiquitin‐conjugating enzyme E2–25k and proteasome subunit alpha type 5. Proteasome inhibitor MG‐132 significantly reduced expression of TGF‐β1 and vimentin. PLpro upregulated HSP27, linking with activation of p38 MAPK and ERK1/2 signaling. Treatment with SB203580 and U0126 reduced PLpro‐induced expression of TGF‐β1, vimentin, and type I collagen. Results point to SARS‐CoV PLpro triggering TGF‐β1 production via ubiquitin proteasome, p38 MAPK, and ERK1/2‐mediated signaling.</div></front></TEI></ISTEX><PMC><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Correlation between <styled-content style="fixed-case" toggle="no">TGF</styled-content>‐β1 expression and proteomic profiling induced by severe acute respiratory syndrome coronavirus papain‐like protease</title><author><name sortKey="Li, Shih En" sort="Li, Shih En" uniqKey="Li S" first="Shih-Wen" last="Li">Shih-Wen Li</name><affiliation><nlm:aff id="pmic7222-aff-0001"></nlm:aff></affiliation><affiliation><nlm:aff id="pmic7222-aff-0002"></nlm:aff></affiliation></author><author><name sortKey="Yang, Tsuey Hing" sort="Yang, Tsuey Hing" uniqKey="Yang T" first="Tsuey-Ching" last="Yang">Tsuey-Ching Yang</name><affiliation><nlm:aff id="pmic7222-aff-0003"></nlm:aff></affiliation></author><author><name sortKey="Wan, Lei" sort="Wan, Lei" uniqKey="Wan L" first="Lei" last="Wan">Lei Wan</name><affiliation><nlm:aff id="pmic7222-aff-0004"></nlm:aff></affiliation></author><author><name sortKey="Lin, Ying U" sort="Lin, Ying U" uniqKey="Lin Y" first="Ying-Ju" last="Lin">Ying-Ju Lin</name><affiliation><nlm:aff id="pmic7222-aff-0004"></nlm:aff></affiliation></author><author><name sortKey="Tsai, Fuu En" sort="Tsai, Fuu En" uniqKey="Tsai F" first="Fuu-Jen" last="Tsai">Fuu-Jen Tsai</name><affiliation><nlm:aff id="pmic7222-aff-0004"></nlm:aff></affiliation></author><author><name sortKey="Lai, Chien Hen" sort="Lai, Chien Hen" uniqKey="Lai C" first="Chien-Chen" last="Lai">Chien-Chen Lai</name><affiliation><nlm:aff id="pmic7222-aff-0002"></nlm:aff></affiliation><affiliation><nlm:aff id="pmic7222-aff-0004"></nlm:aff></affiliation></author><author><name sortKey="Lin, Cheng En" sort="Lin, Cheng En" uniqKey="Lin C" first="Cheng-Wen" last="Lin">Cheng-Wen Lin</name><affiliation><nlm:aff id="pmic7222-aff-0001"></nlm:aff></affiliation><affiliation><nlm:aff 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type="wicri:Area/Ncbi/Checkpoint">003D90</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Correlation between <styled-content style="fixed-case" toggle="no">TGF</styled-content>‐β1 expression and proteomic profiling induced by severe acute respiratory syndrome coronavirus papain‐like protease</title><author><name sortKey="Li, Shih En" sort="Li, Shih En" uniqKey="Li S" first="Shih-Wen" last="Li">Shih-Wen Li</name><affiliation><nlm:aff id="pmic7222-aff-0001"></nlm:aff></affiliation><affiliation><nlm:aff id="pmic7222-aff-0002"></nlm:aff></affiliation></author><author><name sortKey="Yang, Tsuey Hing" sort="Yang, Tsuey Hing" uniqKey="Yang T" first="Tsuey-Ching" last="Yang">Tsuey-Ching Yang</name><affiliation><nlm:aff id="pmic7222-aff-0003"></nlm:aff></affiliation></author><author><name sortKey="Wan, Lei" sort="Wan, Lei" uniqKey="Wan L" first="Lei" last="Wan">Lei Wan</name><affiliation><nlm:aff id="pmic7222-aff-0004"></nlm:aff></affiliation></author><author><name sortKey="Lin, Ying U" sort="Lin, Ying U" uniqKey="Lin Y" first="Ying-Ju" last="Lin">Ying-Ju Lin</name><affiliation><nlm:aff id="pmic7222-aff-0004"></nlm:aff></affiliation></author><author><name sortKey="Tsai, Fuu En" sort="Tsai, Fuu En" uniqKey="Tsai F" first="Fuu-Jen" last="Tsai">Fuu-Jen Tsai</name><affiliation><nlm:aff id="pmic7222-aff-0004"></nlm:aff></affiliation></author><author><name sortKey="Lai, Chien Hen" sort="Lai, Chien Hen" uniqKey="Lai C" first="Chien-Chen" last="Lai">Chien-Chen Lai</name><affiliation><nlm:aff id="pmic7222-aff-0002"></nlm:aff></affiliation><affiliation><nlm:aff id="pmic7222-aff-0004"></nlm:aff></affiliation></author><author><name sortKey="Lin, Cheng En" sort="Lin, Cheng En" uniqKey="Lin C" first="Cheng-Wen" last="Lin">Cheng-Wen Lin</name><affiliation><nlm:aff id="pmic7222-aff-0001"></nlm:aff></affiliation><affiliation><nlm:aff id="pmic7222-aff-0005"></nlm:aff></affiliation><affiliation><nlm:aff id="pmic7222-aff-0006"></nlm:aff></affiliation></author></analytic><series><title level="j">Proteomics</title><idno type="ISSN">1615-9853</idno><idno type="eISSN">1615-9861</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Severe acute respiratory syndrome (<styled-content style="fixed-case" toggle="no">SARS</styled-content>) coronavirus (<styled-content style="fixed-case" toggle="no">SARS</styled-content>‐<styled-content style="fixed-case" toggle="no">C</styled-content>o<styled-content style="fixed-case" toggle="no">V</styled-content>) papain‐like protease (<styled-content style="fixed-case" toggle="no">PL</styled-content>pro), a deubiquitinating enzyme, demonstrates inactivation of interferon (<styled-content style="fixed-case" toggle="no">IFN</styled-content>) regulatory factor 3 and <styled-content style="fixed-case" toggle="no">NF</styled-content>‐κ<styled-content style="fixed-case" toggle="no">B</styled-content>, reduction of IFN induction, and suppression of type I <styled-content style="fixed-case" toggle="no">IFN</styled-content> signaling pathway. This study investigates cytokine expression and proteomic change induced by <styled-content style="fixed-case" toggle="no">SARS</styled-content>‐<styled-content style="fixed-case" toggle="no">C</styled-content>o<styled-content style="fixed-case" toggle="no">V PL</styled-content>pro in human promonocyte cells. PLpro significantly increased <styled-content style="fixed-case" toggle="no">TGF</styled-content>‐β1 m<styled-content style="fixed-case" toggle="no">RNA</styled-content> expression (greater than fourfold) and protein production (greater than threefold). Proteomic analysis, <styled-content style="fixed-case" toggle="no">W</styled-content>estern blot, and quantitative real‐time <styled-content style="fixed-case" toggle="no">PCR</styled-content> assays indicated <styled-content style="fixed-case" toggle="no">PL</styled-content>pro upregulating <styled-content style="fixed-case" toggle="no">TGF</styled-content>‐β1‐associated genes: <styled-content style="fixed-case" toggle="no">HSP</styled-content>27, protein disulfide isomerase <styled-content style="fixed-case" toggle="no">A</styled-content>3 precursor, glial fibrillary acidic protein, vimentin, retinal dehydrogenase 2, and glutathione transferase omega‐1. PLpro‐activated ubiquitin proteasome pathway via upregulation of ubiquitin‐conjugating enzyme <styled-content style="fixed-case" toggle="no">E</styled-content>2–25k and proteasome subunit alpha type 5. Proteasome inhibitor <styled-content style="fixed-case" toggle="no">MG</styled-content>‐132 significantly reduced expression of <styled-content style="fixed-case" toggle="no">TGF</styled-content>‐β1 and vimentin. <styled-content style="fixed-case" toggle="no">PL</styled-content>pro upregulated <styled-content style="fixed-case" toggle="no">HSP</styled-content>27, linking with activation of p38 <styled-content style="fixed-case" toggle="no">MAPK</styled-content> and <styled-content style="fixed-case" toggle="no">ERK</styled-content>1/2 signaling. Treatment with <styled-content style="fixed-case" toggle="no">SB</styled-content>203580 and <styled-content style="fixed-case" toggle="no">U</styled-content>0126 reduced <styled-content style="fixed-case" toggle="no">PL</styled-content>pro‐induced expression of <styled-content style="fixed-case" toggle="no">TGF</styled-content>‐β1, vimentin, and type I collagen. Results point to <styled-content style="fixed-case" toggle="no">SARS</styled-content>‐<styled-content style="fixed-case" toggle="no">C</styled-content>o<styled-content style="fixed-case" toggle="no">V PL</styled-content>pro triggering <styled-content style="fixed-case" toggle="no">TGF</styled-content>‐β1 production via ubiquitin proteasome, p38 <styled-content style="fixed-case" toggle="no">MAPK</styled-content>, and <styled-content style="fixed-case" toggle="no">ERK</styled-content>1/2‐mediated signaling.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct></listBibl></div1></back></TEI></PMC></double></record>Pour manipuler ce document sous Unix (Dilib)
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