Iridovirus CARD Protein Inhibits Apoptosis through Intrinsic and Extrinsic Pathways
Grouper iridovirus (GIV) belongs to the genus Ranavirus of the family Iridoviridae; the genomes of such viruses contain an anti-apoptotic caspase recruitment domain (CARD) gene. The GIV-CARD gene encodes a protein of 91 amino acids with a molecular mass of 10,505 Daltons, and shows high similarity t...
Gespeichert in:
| Veröffentlicht in: | PloS one 2015-06, Vol.10 (6), p.e0129071-e0129071 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e0129071 |
|---|---|
| container_issue | 6 |
| container_start_page | e0129071 |
| container_title | PloS one |
| container_volume | 10 |
| creator | Chen, Chien-Wen Wu, Ming-Shan Huang, Yi-Jen Lin, Pei-Wen Shih, Chueh-Ju Lin, Fu-Pang Chang, Chi-Yao |
| description | Grouper iridovirus (GIV) belongs to the genus Ranavirus of the family Iridoviridae; the genomes of such viruses contain an anti-apoptotic caspase recruitment domain (CARD) gene. The GIV-CARD gene encodes a protein of 91 amino acids with a molecular mass of 10,505 Daltons, and shows high similarity to other viral CARD genes and human ICEBERG. In this study, we used Northern blot to demonstrate that GIV-CARD transcription begins at 4 h post-infection; furthermore, we report that its transcription is completely inhibited by cycloheximide but not by aphidicolin, indicating that GIV-CARD is an early gene. GIV-CARD-EGFP and GIV-CARD-FLAG recombinant proteins were observed to translocate from the cytoplasm into the nucleus, but no obvious nuclear localization sequence was observed within GIV-CARD. RNA interference-mediated knockdown of GIV-CARD in GK cells infected with GIV inhibited expression of GIV-CARD and five other viral genes during the early stages of infection, and also reduced GIV infection ability. Immunostaining was performed to show that apoptosis was effectively inhibited in cells expressing GIV-CARD. HeLa cells irradiated with UV or treated with anti-Fas antibody will undergo apoptosis through the intrinsic and extrinsic pathways, respectively. However, over-expression of recombinant GIV-CARD protein in HeLa cells inhibited apoptosis induced by mitochondrial and death receptor signaling. Finally, we report that expression of GIV-CARD in HeLa cells significantly reduced the activities of caspase-8 and -9 following apoptosis triggered by anti-Fas antibody. Taken together, these results demonstrate that GIV-CARD inhibits apoptosis through both intrinsic and extrinsic pathways. |
| doi_str_mv | 10.1371/journal.pone.0129071 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_1686215106</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A416664927</galeid><doaj_id>oai_doaj_org_article_84c199ea9af74851b4c218efff798fb6</doaj_id><sourcerecordid>A416664927</sourcerecordid><originalsourceid>FETCH-LOGICAL-c692t-d07bdf6753d648c06034698f052fabd49283874925cb0f753a4b12f4b80a80213</originalsourceid><addsrcrecordid>eNqNkl1v0zAYhSMEYqPwDxBEQkJw0eKvOPYNUlUGVJq0aQNuLcexG1dp3NnO2P49Lk2nBu0C-cKO_bzHfk9Olr2GYAZxCT-tXe872c62rtMzABEHJXySnUKO0ZQigJ8erU-yFyGsASgwo_R5doIoICXG-DS7Xnpbu1vr-5Av5ldf8kvvorZdvuwaW9kY8vnWbaMLNuSx8a5fNekoetsFq3LZ1fnZ3eHrUsbmt7wPL7NnRrZBvxrmSfbz69mPxffp-cW35WJ-PlWUozitQVnVhpYFrilhClCACeXMgAIZWdWEI4ZZmaZCVcAkTJIKIkMqBiQDCOJJ9navu21dEIMfQUDKKIIFBDQRyz1RO7kWW2830t8LJ634u-H8SkgfrWq1YERBzrXk0pSEFbAiCkGmjTFlelO10_o83NZXG10rnVyQ7Uh0fNLZRqzcrSCkKDnaCXwYBLy76XWIYmOD0m0rO-36_bs55yy1Pcne_YM-3t1ArWRqwHbGpXvVTlTMCaSUJu_KRM0eodKo9caqFB5j0_6o4OOoIDFR38WV7EMQy-ur_2cvfo3Z90dso2Ubm-DaPlrXhTFI9qDyLgSvzYPJEIhd9g9uiF32xZD9VPbm-Ac9FB3Cjv8Aj7v9pQ</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1686215106</pqid></control><display><type>article</type><title>Iridovirus CARD Protein Inhibits Apoptosis through Intrinsic and Extrinsic Pathways</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Public Library of Science (PLoS) Journals Open Access</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Chen, Chien-Wen ; Wu, Ming-Shan ; Huang, Yi-Jen ; Lin, Pei-Wen ; Shih, Chueh-Ju ; Lin, Fu-Pang ; Chang, Chi-Yao</creator><contributor>Srinivasula, Srinivasa M</contributor><creatorcontrib>Chen, Chien-Wen ; Wu, Ming-Shan ; Huang, Yi-Jen ; Lin, Pei-Wen ; Shih, Chueh-Ju ; Lin, Fu-Pang ; Chang, Chi-Yao ; Srinivasula, Srinivasa M</creatorcontrib><description>Grouper iridovirus (GIV) belongs to the genus Ranavirus of the family Iridoviridae; the genomes of such viruses contain an anti-apoptotic caspase recruitment domain (CARD) gene. The GIV-CARD gene encodes a protein of 91 amino acids with a molecular mass of 10,505 Daltons, and shows high similarity to other viral CARD genes and human ICEBERG. In this study, we used Northern blot to demonstrate that GIV-CARD transcription begins at 4 h post-infection; furthermore, we report that its transcription is completely inhibited by cycloheximide but not by aphidicolin, indicating that GIV-CARD is an early gene. GIV-CARD-EGFP and GIV-CARD-FLAG recombinant proteins were observed to translocate from the cytoplasm into the nucleus, but no obvious nuclear localization sequence was observed within GIV-CARD. RNA interference-mediated knockdown of GIV-CARD in GK cells infected with GIV inhibited expression of GIV-CARD and five other viral genes during the early stages of infection, and also reduced GIV infection ability. Immunostaining was performed to show that apoptosis was effectively inhibited in cells expressing GIV-CARD. HeLa cells irradiated with UV or treated with anti-Fas antibody will undergo apoptosis through the intrinsic and extrinsic pathways, respectively. However, over-expression of recombinant GIV-CARD protein in HeLa cells inhibited apoptosis induced by mitochondrial and death receptor signaling. Finally, we report that expression of GIV-CARD in HeLa cells significantly reduced the activities of caspase-8 and -9 following apoptosis triggered by anti-Fas antibody. Taken together, these results demonstrate that GIV-CARD inhibits apoptosis through both intrinsic and extrinsic pathways.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0129071</identifier><identifier>PMID: 26047333</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Amino Acid Sequence ; Amino acids ; Animals ; Aphidicolin ; Apoptosis ; Base Sequence ; Biotechnology ; CARD Signaling Adaptor Proteins - chemistry ; CARD Signaling Adaptor Proteins - genetics ; CARD Signaling Adaptor Proteins - metabolism ; Caspase ; Caspase 8 - metabolism ; Caspase 9 - metabolism ; Caspase-8 ; Cell Line ; Cellular biology ; Cycloheximide ; Cycloheximide - pharmacology ; Cytoplasm ; Epinephelus awoara ; Fisheries ; Fishes ; Gene expression ; Genes ; Genes, Viral ; Genomes ; Genomics ; Health aspects ; HeLa Cells ; Herpes viruses ; Humans ; Infection ; Infections ; Inhibition ; Iridovirus - genetics ; Iridovirus - metabolism ; Laboratories ; Localization ; Mitochondria ; Models, Molecular ; Molecular chains ; Molecular Sequence Data ; Nuclei ; Nucleotide sequence ; Overexpression ; Pathways ; Perciformes - virology ; Protein Synthesis Inhibitors - pharmacology ; Proteins ; Reptiles & amphibians ; Ribonucleic acid ; RNA ; RNA-mediated interference ; Sequence Alignment ; Signal transduction ; Transcription ; Transcriptional Activation - drug effects ; Up-Regulation ; Vaccines ; Viral infections ; Viral Proteins - chemistry ; Viral Proteins - genetics ; Viral Proteins - metabolism ; Virology ; Viruses</subject><ispartof>PloS one, 2015-06, Vol.10 (6), p.e0129071-e0129071</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Chen et al 2015 Chen et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-d07bdf6753d648c06034698f052fabd49283874925cb0f753a4b12f4b80a80213</citedby><cites>FETCH-LOGICAL-c692t-d07bdf6753d648c06034698f052fabd49283874925cb0f753a4b12f4b80a80213</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4457926/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4457926/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26047333$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Srinivasula, Srinivasa M</contributor><creatorcontrib>Chen, Chien-Wen</creatorcontrib><creatorcontrib>Wu, Ming-Shan</creatorcontrib><creatorcontrib>Huang, Yi-Jen</creatorcontrib><creatorcontrib>Lin, Pei-Wen</creatorcontrib><creatorcontrib>Shih, Chueh-Ju</creatorcontrib><creatorcontrib>Lin, Fu-Pang</creatorcontrib><creatorcontrib>Chang, Chi-Yao</creatorcontrib><title>Iridovirus CARD Protein Inhibits Apoptosis through Intrinsic and Extrinsic Pathways</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Grouper iridovirus (GIV) belongs to the genus Ranavirus of the family Iridoviridae; the genomes of such viruses contain an anti-apoptotic caspase recruitment domain (CARD) gene. The GIV-CARD gene encodes a protein of 91 amino acids with a molecular mass of 10,505 Daltons, and shows high similarity to other viral CARD genes and human ICEBERG. In this study, we used Northern blot to demonstrate that GIV-CARD transcription begins at 4 h post-infection; furthermore, we report that its transcription is completely inhibited by cycloheximide but not by aphidicolin, indicating that GIV-CARD is an early gene. GIV-CARD-EGFP and GIV-CARD-FLAG recombinant proteins were observed to translocate from the cytoplasm into the nucleus, but no obvious nuclear localization sequence was observed within GIV-CARD. RNA interference-mediated knockdown of GIV-CARD in GK cells infected with GIV inhibited expression of GIV-CARD and five other viral genes during the early stages of infection, and also reduced GIV infection ability. Immunostaining was performed to show that apoptosis was effectively inhibited in cells expressing GIV-CARD. HeLa cells irradiated with UV or treated with anti-Fas antibody will undergo apoptosis through the intrinsic and extrinsic pathways, respectively. However, over-expression of recombinant GIV-CARD protein in HeLa cells inhibited apoptosis induced by mitochondrial and death receptor signaling. Finally, we report that expression of GIV-CARD in HeLa cells significantly reduced the activities of caspase-8 and -9 following apoptosis triggered by anti-Fas antibody. Taken together, these results demonstrate that GIV-CARD inhibits apoptosis through both intrinsic and extrinsic pathways.</description><subject>Amino Acid Sequence</subject><subject>Amino acids</subject><subject>Animals</subject><subject>Aphidicolin</subject><subject>Apoptosis</subject><subject>Base Sequence</subject><subject>Biotechnology</subject><subject>CARD Signaling Adaptor Proteins - chemistry</subject><subject>CARD Signaling Adaptor Proteins - genetics</subject><subject>CARD Signaling Adaptor Proteins - metabolism</subject><subject>Caspase</subject><subject>Caspase 8 - metabolism</subject><subject>Caspase 9 - metabolism</subject><subject>Caspase-8</subject><subject>Cell Line</subject><subject>Cellular biology</subject><subject>Cycloheximide</subject><subject>Cycloheximide - pharmacology</subject><subject>Cytoplasm</subject><subject>Epinephelus awoara</subject><subject>Fisheries</subject><subject>Fishes</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genes, Viral</subject><subject>Genomes</subject><subject>Genomics</subject><subject>Health aspects</subject><subject>HeLa Cells</subject><subject>Herpes viruses</subject><subject>Humans</subject><subject>Infection</subject><subject>Infections</subject><subject>Inhibition</subject><subject>Iridovirus - genetics</subject><subject>Iridovirus - metabolism</subject><subject>Laboratories</subject><subject>Localization</subject><subject>Mitochondria</subject><subject>Models, Molecular</subject><subject>Molecular chains</subject><subject>Molecular Sequence Data</subject><subject>Nuclei</subject><subject>Nucleotide sequence</subject><subject>Overexpression</subject><subject>Pathways</subject><subject>Perciformes - virology</subject><subject>Protein Synthesis Inhibitors - pharmacology</subject><subject>Proteins</subject><subject>Reptiles & amphibians</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA-mediated interference</subject><subject>Sequence Alignment</subject><subject>Signal transduction</subject><subject>Transcription</subject><subject>Transcriptional Activation - drug effects</subject><subject>Up-Regulation</subject><subject>Vaccines</subject><subject>Viral infections</subject><subject>Viral Proteins - chemistry</subject><subject>Viral Proteins - genetics</subject><subject>Viral Proteins - metabolism</subject><subject>Virology</subject><subject>Viruses</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl1v0zAYhSMEYqPwDxBEQkJw0eKvOPYNUlUGVJq0aQNuLcexG1dp3NnO2P49Lk2nBu0C-cKO_bzHfk9Olr2GYAZxCT-tXe872c62rtMzABEHJXySnUKO0ZQigJ8erU-yFyGsASgwo_R5doIoICXG-DS7Xnpbu1vr-5Av5ldf8kvvorZdvuwaW9kY8vnWbaMLNuSx8a5fNekoetsFq3LZ1fnZ3eHrUsbmt7wPL7NnRrZBvxrmSfbz69mPxffp-cW35WJ-PlWUozitQVnVhpYFrilhClCACeXMgAIZWdWEI4ZZmaZCVcAkTJIKIkMqBiQDCOJJ9navu21dEIMfQUDKKIIFBDQRyz1RO7kWW2830t8LJ634u-H8SkgfrWq1YERBzrXk0pSEFbAiCkGmjTFlelO10_o83NZXG10rnVyQ7Uh0fNLZRqzcrSCkKDnaCXwYBLy76XWIYmOD0m0rO-36_bs55yy1Pcne_YM-3t1ArWRqwHbGpXvVTlTMCaSUJu_KRM0eodKo9caqFB5j0_6o4OOoIDFR38WV7EMQy-ur_2cvfo3Z90dso2Ubm-DaPlrXhTFI9qDyLgSvzYPJEIhd9g9uiF32xZD9VPbm-Ac9FB3Cjv8Aj7v9pQ</recordid><startdate>20150605</startdate><enddate>20150605</enddate><creator>Chen, Chien-Wen</creator><creator>Wu, Ming-Shan</creator><creator>Huang, Yi-Jen</creator><creator>Lin, Pei-Wen</creator><creator>Shih, Chueh-Ju</creator><creator>Lin, Fu-Pang</creator><creator>Chang, Chi-Yao</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150605</creationdate><title>Iridovirus CARD Protein Inhibits Apoptosis through Intrinsic and Extrinsic Pathways</title><author>Chen, Chien-Wen ; Wu, Ming-Shan ; Huang, Yi-Jen ; Lin, Pei-Wen ; Shih, Chueh-Ju ; Lin, Fu-Pang ; Chang, Chi-Yao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-d07bdf6753d648c06034698f052fabd49283874925cb0f753a4b12f4b80a80213</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Amino Acid Sequence</topic><topic>Amino acids</topic><topic>Animals</topic><topic>Aphidicolin</topic><topic>Apoptosis</topic><topic>Base Sequence</topic><topic>Biotechnology</topic><topic>CARD Signaling Adaptor Proteins - chemistry</topic><topic>CARD Signaling Adaptor Proteins - genetics</topic><topic>CARD Signaling Adaptor Proteins - metabolism</topic><topic>Caspase</topic><topic>Caspase 8 - metabolism</topic><topic>Caspase 9 - metabolism</topic><topic>Caspase-8</topic><topic>Cell Line</topic><topic>Cellular biology</topic><topic>Cycloheximide</topic><topic>Cycloheximide - pharmacology</topic><topic>Cytoplasm</topic><topic>Epinephelus awoara</topic><topic>Fisheries</topic><topic>Fishes</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Genes, Viral</topic><topic>Genomes</topic><topic>Genomics</topic><topic>Health aspects</topic><topic>HeLa Cells</topic><topic>Herpes viruses</topic><topic>Humans</topic><topic>Infection</topic><topic>Infections</topic><topic>Inhibition</topic><topic>Iridovirus - genetics</topic><topic>Iridovirus - metabolism</topic><topic>Laboratories</topic><topic>Localization</topic><topic>Mitochondria</topic><topic>Models, Molecular</topic><topic>Molecular chains</topic><topic>Molecular Sequence Data</topic><topic>Nuclei</topic><topic>Nucleotide sequence</topic><topic>Overexpression</topic><topic>Pathways</topic><topic>Perciformes - virology</topic><topic>Protein Synthesis Inhibitors - pharmacology</topic><topic>Proteins</topic><topic>Reptiles & amphibians</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA-mediated interference</topic><topic>Sequence Alignment</topic><topic>Signal transduction</topic><topic>Transcription</topic><topic>Transcriptional Activation - drug effects</topic><topic>Up-Regulation</topic><topic>Vaccines</topic><topic>Viral infections</topic><topic>Viral Proteins - chemistry</topic><topic>Viral Proteins - genetics</topic><topic>Viral Proteins - metabolism</topic><topic>Virology</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Chien-Wen</creatorcontrib><creatorcontrib>Wu, Ming-Shan</creatorcontrib><creatorcontrib>Huang, Yi-Jen</creatorcontrib><creatorcontrib>Lin, Pei-Wen</creatorcontrib><creatorcontrib>Shih, Chueh-Ju</creatorcontrib><creatorcontrib>Lin, Fu-Pang</creatorcontrib><creatorcontrib>Chang, Chi-Yao</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Chien-Wen</au><au>Wu, Ming-Shan</au><au>Huang, Yi-Jen</au><au>Lin, Pei-Wen</au><au>Shih, Chueh-Ju</au><au>Lin, Fu-Pang</au><au>Chang, Chi-Yao</au><au>Srinivasula, Srinivasa M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Iridovirus CARD Protein Inhibits Apoptosis through Intrinsic and Extrinsic Pathways</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-06-05</date><risdate>2015</risdate><volume>10</volume><issue>6</issue><spage>e0129071</spage><epage>e0129071</epage><pages>e0129071-e0129071</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Grouper iridovirus (GIV) belongs to the genus Ranavirus of the family Iridoviridae; the genomes of such viruses contain an anti-apoptotic caspase recruitment domain (CARD) gene. The GIV-CARD gene encodes a protein of 91 amino acids with a molecular mass of 10,505 Daltons, and shows high similarity to other viral CARD genes and human ICEBERG. In this study, we used Northern blot to demonstrate that GIV-CARD transcription begins at 4 h post-infection; furthermore, we report that its transcription is completely inhibited by cycloheximide but not by aphidicolin, indicating that GIV-CARD is an early gene. GIV-CARD-EGFP and GIV-CARD-FLAG recombinant proteins were observed to translocate from the cytoplasm into the nucleus, but no obvious nuclear localization sequence was observed within GIV-CARD. RNA interference-mediated knockdown of GIV-CARD in GK cells infected with GIV inhibited expression of GIV-CARD and five other viral genes during the early stages of infection, and also reduced GIV infection ability. Immunostaining was performed to show that apoptosis was effectively inhibited in cells expressing GIV-CARD. HeLa cells irradiated with UV or treated with anti-Fas antibody will undergo apoptosis through the intrinsic and extrinsic pathways, respectively. However, over-expression of recombinant GIV-CARD protein in HeLa cells inhibited apoptosis induced by mitochondrial and death receptor signaling. Finally, we report that expression of GIV-CARD in HeLa cells significantly reduced the activities of caspase-8 and -9 following apoptosis triggered by anti-Fas antibody. Taken together, these results demonstrate that GIV-CARD inhibits apoptosis through both intrinsic and extrinsic pathways.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26047333</pmid><doi>10.1371/journal.pone.0129071</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2015-06, Vol.10 (6), p.e0129071-e0129071 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1686215106 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS) Journals Open Access; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Amino Acid Sequence Amino acids Animals Aphidicolin Apoptosis Base Sequence Biotechnology CARD Signaling Adaptor Proteins - chemistry CARD Signaling Adaptor Proteins - genetics CARD Signaling Adaptor Proteins - metabolism Caspase Caspase 8 - metabolism Caspase 9 - metabolism Caspase-8 Cell Line Cellular biology Cycloheximide Cycloheximide - pharmacology Cytoplasm Epinephelus awoara Fisheries Fishes Gene expression Genes Genes, Viral Genomes Genomics Health aspects HeLa Cells Herpes viruses Humans Infection Infections Inhibition Iridovirus - genetics Iridovirus - metabolism Laboratories Localization Mitochondria Models, Molecular Molecular chains Molecular Sequence Data Nuclei Nucleotide sequence Overexpression Pathways Perciformes - virology Protein Synthesis Inhibitors - pharmacology Proteins Reptiles & amphibians Ribonucleic acid RNA RNA-mediated interference Sequence Alignment Signal transduction Transcription Transcriptional Activation - drug effects Up-Regulation Vaccines Viral infections Viral Proteins - chemistry Viral Proteins - genetics Viral Proteins - metabolism Virology Viruses |
| title | Iridovirus CARD Protein Inhibits Apoptosis through Intrinsic and Extrinsic Pathways |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-19T20%3A15%3A05IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Iridovirus%20CARD%20Protein%20Inhibits%20Apoptosis%20through%20Intrinsic%20and%20Extrinsic%20Pathways&rft.jtitle=PloS%20one&rft.au=Chen,%20Chien-Wen&rft.date=2015-06-05&rft.volume=10&rft.issue=6&rft.spage=e0129071&rft.epage=e0129071&rft.pages=e0129071-e0129071&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0129071&rft_dat=%3Cgale_plos_%3EA416664927%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1686215106&rft_id=info:pmid/26047333&rft_galeid=A416664927&rft_doaj_id=oai_doaj_org_article_84c199ea9af74851b4c218efff798fb6&rfr_iscdi=true |