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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Endolysosomal trafficking of viral G protein-coupled receptor functions in innate immunity and control of viral oncogenesis</title><author><name sortKey="Dong, Xiaonan" sort="Dong, Xiaonan" uniqKey="Dong X" first="Xiaonan" last="Dong">Xiaonan Dong</name><affiliation><nlm:aff id="aff1">Department of Internal Medicine, Center for Autophagy Research,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation></author><author><name sortKey="Cheng, Adam" sort="Cheng, Adam" uniqKey="Cheng A" first="Adam" last="Cheng">Adam Cheng</name><affiliation><nlm:aff id="aff1">Department of Internal Medicine, Center for Autophagy Research,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation></author><author><name sortKey="Zou, Zhongju" sort="Zou, Zhongju" uniqKey="Zou Z" first="Zhongju" last="Zou">Zhongju Zou</name><affiliation><nlm:aff id="aff1">Department of Internal Medicine, Center for Autophagy Research,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">Howard Hughes Medical Institute,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation></author><author><name sortKey="Yang, Yih Sheng" sort="Yang, Yih Sheng" uniqKey="Yang Y" first="Yih-Sheng" last="Yang">Yih-Sheng Yang</name><affiliation><nlm:aff id="aff3">Division of Nephrology, Department of Internal Medicine,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation></author><author><name sortKey="Sumpter, Rhea M" sort="Sumpter, Rhea M" uniqKey="Sumpter R" first="Rhea M." last="Sumpter">Rhea M. Sumpter</name><affiliation><nlm:aff id="aff1">Department of Internal Medicine, Center for Autophagy Research,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation></author><author><name sortKey="Huang, Chou Long" sort="Huang, Chou Long" uniqKey="Huang C" first="Chou-Long" last="Huang">Chou-Long Huang</name><affiliation><nlm:aff id="aff3">Division of Nephrology, Department of Internal Medicine,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation></author><author><name sortKey="Bhagat, Govind" sort="Bhagat, Govind" uniqKey="Bhagat G" first="Govind" last="Bhagat">Govind Bhagat</name><affiliation><nlm:aff id="aff4">Department of Pathology and Cell Biology,<institution>Columbia University Medical Center and New York Presbyterian Hospital</institution>, New York,<addr-line>NY</addr-line> 10032;</nlm:aff></affiliation></author><author><name sortKey="Virgin, Herbert W" sort="Virgin, Herbert W" uniqKey="Virgin H" first="Herbert W." last="Virgin">Herbert W. Virgin</name><affiliation><nlm:aff id="aff5">Department of Pathology and Immunology,<institution>Washington University School of Medicine</institution>, St. Louis,<addr-line>MO</addr-line> 63110;</nlm:aff></affiliation></author><author><name sortKey="Lira, Sergio A" sort="Lira, Sergio A" uniqKey="Lira S" first="Sergio A." last="Lira">Sergio A. Lira</name><affiliation><nlm:aff id="aff6">Immunology Institute,<institution>Icahn School of Medicine at Mount Sinai</institution>, New York,<addr-line>NY</addr-line> 10029;</nlm:aff></affiliation></author><author><name sortKey="Levine, Beth" sort="Levine, Beth" uniqKey="Levine B" first="Beth" last="Levine">Beth Levine</name><affiliation><nlm:aff id="aff1">Department of Internal Medicine, Center for Autophagy Research,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">Howard Hughes Medical Institute,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation><affiliation><nlm:aff id="aff7">Department of Microbiology,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">26929373</idno><idno type="pmc">4801257</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4801257</idno><idno type="RBID">PMC:4801257</idno><idno type="doi">10.1073/pnas.1601860113</idno><date when="2016">2016</date><idno type="wicri:Area/Pmc/Corpus">000698</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000698</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Endolysosomal trafficking of viral G protein-coupled receptor functions in innate immunity and control of viral oncogenesis</title><author><name sortKey="Dong, Xiaonan" sort="Dong, Xiaonan" uniqKey="Dong X" first="Xiaonan" last="Dong">Xiaonan Dong</name><affiliation><nlm:aff id="aff1">Department of Internal Medicine, Center for Autophagy Research,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation></author><author><name sortKey="Cheng, Adam" sort="Cheng, Adam" uniqKey="Cheng A" first="Adam" last="Cheng">Adam Cheng</name><affiliation><nlm:aff id="aff1">Department of Internal Medicine, Center for Autophagy Research,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation></author><author><name sortKey="Zou, Zhongju" sort="Zou, Zhongju" uniqKey="Zou Z" first="Zhongju" last="Zou">Zhongju Zou</name><affiliation><nlm:aff id="aff1">Department of Internal Medicine, Center for Autophagy Research,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">Howard Hughes Medical Institute,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation></author><author><name sortKey="Yang, Yih Sheng" sort="Yang, Yih Sheng" uniqKey="Yang Y" first="Yih-Sheng" last="Yang">Yih-Sheng Yang</name><affiliation><nlm:aff id="aff3">Division of Nephrology, Department of Internal Medicine,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation></author><author><name sortKey="Sumpter, Rhea M" sort="Sumpter, Rhea M" uniqKey="Sumpter R" first="Rhea M." last="Sumpter">Rhea M. Sumpter</name><affiliation><nlm:aff id="aff1">Department of Internal Medicine, Center for Autophagy Research,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation></author><author><name sortKey="Huang, Chou Long" sort="Huang, Chou Long" uniqKey="Huang C" first="Chou-Long" last="Huang">Chou-Long Huang</name><affiliation><nlm:aff id="aff3">Division of Nephrology, Department of Internal Medicine,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation></author><author><name sortKey="Bhagat, Govind" sort="Bhagat, Govind" uniqKey="Bhagat G" first="Govind" last="Bhagat">Govind Bhagat</name><affiliation><nlm:aff id="aff4">Department of Pathology and Cell Biology,<institution>Columbia University Medical Center and New York Presbyterian Hospital</institution>, New York,<addr-line>NY</addr-line> 10032;</nlm:aff></affiliation></author><author><name sortKey="Virgin, Herbert W" sort="Virgin, Herbert W" uniqKey="Virgin H" first="Herbert W." last="Virgin">Herbert W. Virgin</name><affiliation><nlm:aff id="aff5">Department of Pathology and Immunology,<institution>Washington University School of Medicine</institution>, St. Louis,<addr-line>MO</addr-line> 63110;</nlm:aff></affiliation></author><author><name sortKey="Lira, Sergio A" sort="Lira, Sergio A" uniqKey="Lira S" first="Sergio A." last="Lira">Sergio A. Lira</name><affiliation><nlm:aff id="aff6">Immunology Institute,<institution>Icahn School of Medicine at Mount Sinai</institution>, New York,<addr-line>NY</addr-line> 10029;</nlm:aff></affiliation></author><author><name sortKey="Levine, Beth" sort="Levine, Beth" uniqKey="Levine B" first="Beth" last="Levine">Beth Levine</name><affiliation><nlm:aff id="aff1">Department of Internal Medicine, Center for Autophagy Research,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation><affiliation><nlm:aff id="aff2">Howard Hughes Medical Institute,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</nlm:aff></affiliation><affiliation><nlm:aff id="aff7">Department of Microbiology,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390</nlm:aff></affiliation></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="ISSN">0027-8424</idno><idno type="eISSN">1091-6490</idno><imprint><date when="2016">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>Significance</title><p>We show that the autophagy-related protein Beclin 2 functions as a newly described cellular regulator of viral G protein-coupled receptors (GPCRs) and as a suppressor of viral GPCR-driven tumorigenesis. Beclin 2 functions in regulating Kaposi’s sarcoma-associated herpesvirus-encoded GPCR levels, proinflammatory signaling, and oncogenic activity in mice by facilitating viral GPCR endolysosomal trafficking. This Beclin 2-dependent endolysosomal trafficking and degradation of an oncogenic viral protein may represent a broader and heretofore unappreciated role of the endolysosomal trafficking machinery in innate immunity (by defending against microbial virulence factors) and in tumor suppression (by degrading oncogenic cell surface receptors).</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Proc Natl Acad Sci U S A</journal-id><journal-id journal-id-type="iso-abbrev">Proc. Natl. Acad. Sci. U.S.A</journal-id><journal-id journal-id-type="hwp">pnas</journal-id><journal-id journal-id-type="pmc">pnas</journal-id><journal-id journal-id-type="publisher-id">PNAS</journal-id><journal-title-group><journal-title>Proceedings of the National Academy of Sciences of the United States of America</journal-title></journal-title-group><issn pub-type="ppub">0027-8424</issn><issn pub-type="epub">1091-6490</issn><publisher><publisher-name>National Academy of Sciences</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">26929373</article-id><article-id pub-id-type="pmc">4801257</article-id><article-id pub-id-type="publisher-id">201601860</article-id><article-id pub-id-type="doi">10.1073/pnas.1601860113</article-id><article-categories><subj-group subj-group-type="heading"><subject>Biological Sciences</subject><subj-group><subject>Immunology and Inflammation</subject></subj-group></subj-group></article-categories><title-group><article-title>Endolysosomal trafficking of viral G protein-coupled receptor functions in innate immunity and control of viral oncogenesis</article-title><alt-title alt-title-type="short">Lysosomal degradation of a viral oncoprotein</alt-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Dong</surname><given-names>Xiaonan</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Cheng</surname><given-names>Adam</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Zou</surname><given-names>Zhongju</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Yang</surname><given-names>Yih-Sheng</given-names></name><xref ref-type="aff" rid="aff3"><sup>c</sup></xref></contrib><contrib contrib-type="author"><name><surname>Sumpter</surname><given-names>Rhea M.</given-names><suffix>Jr.</suffix></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Huang</surname><given-names>Chou-Long</given-names></name><xref ref-type="aff" rid="aff3"><sup>c</sup></xref></contrib><contrib contrib-type="author"><name><surname>Bhagat</surname><given-names>Govind</given-names></name><xref ref-type="aff" rid="aff4"><sup>d</sup></xref></contrib><contrib contrib-type="author"><name><surname>Virgin</surname><given-names>Herbert W.</given-names></name><xref ref-type="aff" rid="aff5"><sup>e</sup></xref></contrib><contrib contrib-type="author"><name><surname>Lira</surname><given-names>Sergio A.</given-names></name><xref ref-type="aff" rid="aff6"><sup>f</sup></xref></contrib><contrib contrib-type="author"><name><surname>Levine</surname><given-names>Beth</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="aff" rid="aff2"><sup>b</sup></xref><xref ref-type="aff" rid="aff7"><sup>g</sup></xref><xref ref-type="corresp" rid="cor1"><sup>1</sup></xref></contrib><aff id="aff1"><sup>a</sup>Department of Internal Medicine, Center for Autophagy Research,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</aff><aff id="aff2"><sup>b</sup>Howard Hughes Medical Institute,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</aff><aff id="aff3"><sup>c</sup>Division of Nephrology, Department of Internal Medicine,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390;</aff><aff id="aff4"><sup>d</sup>Department of Pathology and Cell Biology,<institution>Columbia University Medical Center and New York Presbyterian Hospital</institution>, New York,<addr-line>NY</addr-line> 10032;</aff><aff id="aff5"><sup>e</sup>Department of Pathology and Immunology,<institution>Washington University School of Medicine</institution>, St. Louis,<addr-line>MO</addr-line> 63110;</aff><aff id="aff6"><sup>f</sup>Immunology Institute,<institution>Icahn School of Medicine at Mount Sinai</institution>, New York,<addr-line>NY</addr-line> 10029;</aff><aff id="aff7"><sup>g</sup>Department of Microbiology,<institution>University of Texas Southwestern Medical Center</institution>, Dallas,<addr-line>TX</addr-line> 75390</aff></contrib-group><author-notes><corresp id="cor1"><sup>1</sup>To whom correspondence should be addressed. Email: <email>beth.levine@utsouthwestern.edu</email>.</corresp><fn fn-type="edited-by"><p>Contributed by Beth Levine, February 4, 2016 (sent for review January 13, 2016; reviewed by Karla Kirkegaard and Michael B. A. Oldstone)</p></fn><fn fn-type="con"><p>Author contributions: X.D., H.W.V., S.A.L., and B.L. designed research; X.D., A.C., Z.Z., Y.-S.Y., R.M.S., and C.-L.H. performed research; X.D., G.B., H.W.V., S.A.L., and B.L. analyzed data; and X.D., H.W.V., S.A.L., and B.L. wrote the paper.</p></fn><fn fn-type="con"><p>Reviewers: K.K., Stanford University; and M.B.A.O., The Scripps Research Institute.</p></fn></author-notes><pub-date pub-type="ppub"><day>15</day><month>3</month><year>2016</year></pub-date><pub-date pub-type="epub"><day>29</day><month>2</month><year>2016</year></pub-date><pub-date pub-type="pmc-release"><day>29</day><month>2</month><year>2016</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on the
<volume>113</volume><issue>11</issue><fpage>2994</fpage><lpage>2999</lpage><permissions><license license-type="open-access"><license-p>Freely available online through the PNAS open access option.</license-p></license></permissions><self-uri xlink:title="pdf" xlink:href="pnas.201601860.pdf"></self-uri><abstract abstract-type="executive-summary"><title>Significance</title><p>We show that the autophagy-related protein Beclin 2 functions as a newly described cellular regulator of viral G protein-coupled receptors (GPCRs) and as a suppressor of viral GPCR-driven tumorigenesis. Beclin 2 functions in regulating Kaposi’s sarcoma-associated herpesvirus-encoded GPCR levels, proinflammatory signaling, and oncogenic activity in mice by facilitating viral GPCR endolysosomal trafficking. This Beclin 2-dependent endolysosomal trafficking and degradation of an oncogenic viral protein may represent a broader and heretofore unappreciated role of the endolysosomal trafficking machinery in innate immunity (by defending against microbial virulence factors) and in tumor suppression (by degrading oncogenic cell surface receptors).</p></abstract><abstract><p>The ubiquitin-proteasome system degrades viral oncoproteins and other microbial virulence factors; however, the role of endolysosomal degradation pathways in these processes is unclear. Kaposi’s sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi’s sarcoma, and a constitutively active viral G protein-coupled receptor (vGPCR) contributes to the pathogenesis of KSHV-induced tumors. We report that a recently discovered autophagy-related protein, Beclin 2, interacts with KSHV GPCR, facilitates its endolysosomal degradation, and inhibits vGPCR-driven oncogenic signaling. Furthermore, monoallelic loss of <italic>Becn2</italic> in mice accelerates the progression of vGPCR-induced lesions that resemble human Kaposi’s sarcoma. Taken together, these findings indicate that Beclin 2 is a host antiviral molecule that protects against the pathogenic effects of KSHV GPCR by facilitating its endolysosomal degradation. More broadly, our data suggest a role for host endolysosomal trafficking pathways in regulating viral pathogenesis and oncogenic signaling.</p></abstract><kwd-group><kwd>endolysosomal trafficking</kwd><kwd>Beclin 2</kwd><kwd>autophagy</kwd><kwd>viral GPCR</kwd><kwd>oncogenesis</kwd></kwd-group><funding-group><award-group id="gs1"><funding-source id="sp1">Office of Extramural Research, National Institutes of Health (OER)<named-content content-type="funder-id">100006955</named-content></funding-source><award-id rid="sp1">R01 CA109618</award-id></award-group><award-group id="gs2"><funding-source id="sp2">Office of Extramural Research, National Institutes of Health (OER)<named-content content-type="funder-id">100006955</named-content></funding-source><award-id rid="sp2">U19 AI109725</award-id></award-group><award-group id="gs3"><funding-source id="sp3">Office of Extramural Research, National Institutes of Health (OER)<named-content content-type="funder-id">100006955</named-content></funding-source><award-id rid="sp3">P01 DK072201</award-id></award-group><award-group id="gs4"><funding-source id="sp4">Office of Extramural Research, National Institutes of Health (OER)<named-content content-type="funder-id">100006955</named-content></funding-source><award-id rid="sp4">RO1 CA161373</award-id></award-group><award-group id="gs5"><funding-source id="sp5">Office of Extramural Research, National Institutes of Health (OER)<named-content content-type="funder-id">100006955</named-content></funding-source><award-id rid="sp5">P30 DK079328</award-id></award-group><award-group id="gs6"><funding-source id="sp6">Office of Extramural Research, National Institutes of Health (OER)<named-content content-type="funder-id">100006955</named-content></funding-source><award-id rid="sp6">KO8 AI099150</award-id></award-group><award-group id="gs7"><funding-source id="sp7">Cancer Prevention and Research Institute of Texas (CPRIT)<named-content content-type="funder-id">100004917</named-content></funding-source><award-id rid="sp7">RP 120718</award-id></award-group><award-group id="gs8"><funding-source id="sp8">Burroughs Wellcome Fund (BWF)<named-content content-type="funder-id">100000861</named-content></funding-source><award-id rid="sp8">CMSA</award-id></award-group></funding-group><counts><page-count count="6"></page-count></counts></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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