Tumor necrosis factor induces rapid down-regulation of TXNIP in human T cells
In addition to antigen-driven signals, T cells need co-stimulatory signals for robust activation. Several receptors, including members of the tumor necrosis factor receptor superfamily (TNFRSF), can deliver co-stimulatory signals to T cells. Thioredoxin interacting protein (TXNIP) is an important in...
Gespeichert in:
| Veröffentlicht in: | Scientific reports 2019-11, Vol.9 (1), p.16725-13, Article 16725 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 13 |
|---|---|
| container_issue | 1 |
| container_start_page | 16725 |
| container_title | Scientific reports |
| container_volume | 9 |
| creator | Levring, Trine B. Kongsbak-Wismann, Martin Rode, Anna K. O. Al-Jaberi, Fatima A. H. Lopez, Daniel V. Met, Özcan Woetmann, Anders Bonefeld, Charlotte M. Ødum, Niels Geisler, Carsten |
| description | In addition to antigen-driven signals, T cells need co-stimulatory signals for robust activation. Several receptors, including members of the tumor necrosis factor receptor superfamily (TNFRSF), can deliver co-stimulatory signals to T cells. Thioredoxin interacting protein (TXNIP) is an important inhibitor of glucose uptake and cell proliferation, but it is unknown how TXNIP is regulated in T cells. The aim of this study was to determine expression levels and regulation of TXNIP in human T cells. We found that naïve T cells express high levels of TXNIP and that treatment of blood samples with TNF results in rapid down-regulation of TXNIP in the T cells. TNF-induced TXNIP down-regulation correlated with increased glucose uptake. Furthermore, we found that density gradient centrifugation (DGC) induced down-regulation of TXNIP. We demonstrate that DGC induced TNF production that paralleled the TXNIP down-regulation. Treatment of blood with toll-like receptor (TLR) ligands induced TNF production and TXNIP down-regulation, suggesting that damage-associated molecular patterns (DAMPs), such as endogenous TLR ligands, released during DGC play a role in DGC-induced TXNIP down-regulation. Finally, we demonstrate that TNF-induced TXNIP down-regulation is dependent on caspase activity and is caused by caspase-mediated cleavage of TXNIP. |
| doi_str_mv | 10.1038/s41598-019-53234-x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6853882</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2314558679</sourcerecordid><originalsourceid>FETCH-LOGICAL-c474t-39260204ee182a3c1cef0f0433cf7471e266a3e49b57d5b8e55538d852d474093</originalsourceid><addsrcrecordid>eNp9kUtLxDAQx4MoKuoX8CABL16qebbpRRDxBb4OK3gL2XS6VtpkTVpdv71Z1_fBXJJhfvOfmfwR2qZknxKuDqKgslQZoWUmOeMimy2hdUaEzBhnbPnHew1txfhI0pGsFLRcRWucFilD-Dq6Gg2dD9iBDT42EdfG9iluXDVYiDiYaVPhyr-4LMBkaE3feId9jUf31xe3CcMPQ2ccHmELbRs30Upt2ghbH_cGujs9GR2fZ5c3ZxfHR5eZFYXoM16ynKT5AKhihltqoSY1EZzbuhAFBZbnhoMox7Ko5FiBlJKrSklWpXpS8g10uNCdDuMOKguuD6bV09B0Jrxqbxr9O-OaBz3xzzpXSUixJLD3IRD80wCx110T5ysYB36ImnEqpFR5Me-1-wd99ENwab13ilMpC5IotqDm_xgD1F_DUKLnhumFYToZpt8N07NUtPNzja-ST3sSwBdATCk3gfDd-x_ZN9IGoDo</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2314315570</pqid></control><display><type>article</type><title>Tumor necrosis factor induces rapid down-regulation of TXNIP in human T cells</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Springer Nature OA Free Journals</source><source>Nature Free</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>Free Full-Text Journals in Chemistry</source><creator>Levring, Trine B. ; Kongsbak-Wismann, Martin ; Rode, Anna K. O. ; Al-Jaberi, Fatima A. H. ; Lopez, Daniel V. ; Met, Özcan ; Woetmann, Anders ; Bonefeld, Charlotte M. ; Ødum, Niels ; Geisler, Carsten</creator><creatorcontrib>Levring, Trine B. ; Kongsbak-Wismann, Martin ; Rode, Anna K. O. ; Al-Jaberi, Fatima A. H. ; Lopez, Daniel V. ; Met, Özcan ; Woetmann, Anders ; Bonefeld, Charlotte M. ; Ødum, Niels ; Geisler, Carsten</creatorcontrib><description>In addition to antigen-driven signals, T cells need co-stimulatory signals for robust activation. Several receptors, including members of the tumor necrosis factor receptor superfamily (TNFRSF), can deliver co-stimulatory signals to T cells. Thioredoxin interacting protein (TXNIP) is an important inhibitor of glucose uptake and cell proliferation, but it is unknown how TXNIP is regulated in T cells. The aim of this study was to determine expression levels and regulation of TXNIP in human T cells. We found that naïve T cells express high levels of TXNIP and that treatment of blood samples with TNF results in rapid down-regulation of TXNIP in the T cells. TNF-induced TXNIP down-regulation correlated with increased glucose uptake. Furthermore, we found that density gradient centrifugation (DGC) induced down-regulation of TXNIP. We demonstrate that DGC induced TNF production that paralleled the TXNIP down-regulation. Treatment of blood with toll-like receptor (TLR) ligands induced TNF production and TXNIP down-regulation, suggesting that damage-associated molecular patterns (DAMPs), such as endogenous TLR ligands, released during DGC play a role in DGC-induced TXNIP down-regulation. Finally, we demonstrate that TNF-induced TXNIP down-regulation is dependent on caspase activity and is caused by caspase-mediated cleavage of TXNIP.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-019-53234-x</identifier><identifier>PMID: 31723203</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 13/95 ; 631/250/1619/554 ; 631/250/516 ; 82 ; 82/80 ; Blood ; Carrier Proteins - antagonists & inhibitors ; Carrier Proteins - genetics ; Carrier Proteins - metabolism ; Caspase ; Cell activation ; Cell proliferation ; Centrifugation ; Down-Regulation ; Glucose - metabolism ; Humanities and Social Sciences ; Humans ; Ligands ; Lymphocytes ; Lymphocytes T ; multidisciplinary ; Necrosis ; Science ; Science (multidisciplinary) ; T-Lymphocytes - drug effects ; T-Lymphocytes - metabolism ; Thioredoxin ; Toll-like receptors ; Toll-Like Receptors - agonists ; Tumor necrosis factor ; Tumor Necrosis Factor-alpha - pharmacology ; Tumor necrosis factor-TNF</subject><ispartof>Scientific reports, 2019-11, Vol.9 (1), p.16725-13, Article 16725</ispartof><rights>The Author(s) 2019</rights><rights>2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-39260204ee182a3c1cef0f0433cf7471e266a3e49b57d5b8e55538d852d474093</citedby><cites>FETCH-LOGICAL-c474t-39260204ee182a3c1cef0f0433cf7471e266a3e49b57d5b8e55538d852d474093</cites><orcidid>0000-0003-2707-9313 ; 0000-0002-8472-0771 ; 0000-0003-3135-5624 ; 0000-0002-0523-6229 ; 0000-0002-3496-9333 ; 0000-0002-3008-735X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6853882/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6853882/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27903,27904,41099,42168,51554,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31723203$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Levring, Trine B.</creatorcontrib><creatorcontrib>Kongsbak-Wismann, Martin</creatorcontrib><creatorcontrib>Rode, Anna K. O.</creatorcontrib><creatorcontrib>Al-Jaberi, Fatima A. H.</creatorcontrib><creatorcontrib>Lopez, Daniel V.</creatorcontrib><creatorcontrib>Met, Özcan</creatorcontrib><creatorcontrib>Woetmann, Anders</creatorcontrib><creatorcontrib>Bonefeld, Charlotte M.</creatorcontrib><creatorcontrib>Ødum, Niels</creatorcontrib><creatorcontrib>Geisler, Carsten</creatorcontrib><title>Tumor necrosis factor induces rapid down-regulation of TXNIP in human T cells</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>In addition to antigen-driven signals, T cells need co-stimulatory signals for robust activation. Several receptors, including members of the tumor necrosis factor receptor superfamily (TNFRSF), can deliver co-stimulatory signals to T cells. Thioredoxin interacting protein (TXNIP) is an important inhibitor of glucose uptake and cell proliferation, but it is unknown how TXNIP is regulated in T cells. The aim of this study was to determine expression levels and regulation of TXNIP in human T cells. We found that naïve T cells express high levels of TXNIP and that treatment of blood samples with TNF results in rapid down-regulation of TXNIP in the T cells. TNF-induced TXNIP down-regulation correlated with increased glucose uptake. Furthermore, we found that density gradient centrifugation (DGC) induced down-regulation of TXNIP. We demonstrate that DGC induced TNF production that paralleled the TXNIP down-regulation. Treatment of blood with toll-like receptor (TLR) ligands induced TNF production and TXNIP down-regulation, suggesting that damage-associated molecular patterns (DAMPs), such as endogenous TLR ligands, released during DGC play a role in DGC-induced TXNIP down-regulation. Finally, we demonstrate that TNF-induced TXNIP down-regulation is dependent on caspase activity and is caused by caspase-mediated cleavage of TXNIP.</description><subject>13</subject><subject>13/95</subject><subject>631/250/1619/554</subject><subject>631/250/516</subject><subject>82</subject><subject>82/80</subject><subject>Blood</subject><subject>Carrier Proteins - antagonists & inhibitors</subject><subject>Carrier Proteins - genetics</subject><subject>Carrier Proteins - metabolism</subject><subject>Caspase</subject><subject>Cell activation</subject><subject>Cell proliferation</subject><subject>Centrifugation</subject><subject>Down-Regulation</subject><subject>Glucose - metabolism</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Ligands</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>multidisciplinary</subject><subject>Necrosis</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>T-Lymphocytes - drug effects</subject><subject>T-Lymphocytes - metabolism</subject><subject>Thioredoxin</subject><subject>Toll-like receptors</subject><subject>Toll-Like Receptors - agonists</subject><subject>Tumor necrosis factor</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Tumor necrosis factor-TNF</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kUtLxDAQx4MoKuoX8CABL16qebbpRRDxBb4OK3gL2XS6VtpkTVpdv71Z1_fBXJJhfvOfmfwR2qZknxKuDqKgslQZoWUmOeMimy2hdUaEzBhnbPnHew1txfhI0pGsFLRcRWucFilD-Dq6Gg2dD9iBDT42EdfG9iluXDVYiDiYaVPhyr-4LMBkaE3feId9jUf31xe3CcMPQ2ccHmELbRs30Upt2ghbH_cGujs9GR2fZ5c3ZxfHR5eZFYXoM16ynKT5AKhihltqoSY1EZzbuhAFBZbnhoMox7Ko5FiBlJKrSklWpXpS8g10uNCdDuMOKguuD6bV09B0Jrxqbxr9O-OaBz3xzzpXSUixJLD3IRD80wCx110T5ysYB36ImnEqpFR5Me-1-wd99ENwab13ilMpC5IotqDm_xgD1F_DUKLnhumFYToZpt8N07NUtPNzja-ST3sSwBdATCk3gfDd-x_ZN9IGoDo</recordid><startdate>20191113</startdate><enddate>20191113</enddate><creator>Levring, Trine B.</creator><creator>Kongsbak-Wismann, Martin</creator><creator>Rode, Anna K. O.</creator><creator>Al-Jaberi, Fatima A. H.</creator><creator>Lopez, Daniel V.</creator><creator>Met, Özcan</creator><creator>Woetmann, Anders</creator><creator>Bonefeld, Charlotte M.</creator><creator>Ødum, Niels</creator><creator>Geisler, Carsten</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-2707-9313</orcidid><orcidid>https://orcid.org/0000-0002-8472-0771</orcidid><orcidid>https://orcid.org/0000-0003-3135-5624</orcidid><orcidid>https://orcid.org/0000-0002-0523-6229</orcidid><orcidid>https://orcid.org/0000-0002-3496-9333</orcidid><orcidid>https://orcid.org/0000-0002-3008-735X</orcidid></search><sort><creationdate>20191113</creationdate><title>Tumor necrosis factor induces rapid down-regulation of TXNIP in human T cells</title><author>Levring, Trine B. ; Kongsbak-Wismann, Martin ; Rode, Anna K. O. ; Al-Jaberi, Fatima A. H. ; Lopez, Daniel V. ; Met, Özcan ; Woetmann, Anders ; Bonefeld, Charlotte M. ; Ødum, Niels ; Geisler, Carsten</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-39260204ee182a3c1cef0f0433cf7471e266a3e49b57d5b8e55538d852d474093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>13</topic><topic>13/95</topic><topic>631/250/1619/554</topic><topic>631/250/516</topic><topic>82</topic><topic>82/80</topic><topic>Blood</topic><topic>Carrier Proteins - antagonists & inhibitors</topic><topic>Carrier Proteins - genetics</topic><topic>Carrier Proteins - metabolism</topic><topic>Caspase</topic><topic>Cell activation</topic><topic>Cell proliferation</topic><topic>Centrifugation</topic><topic>Down-Regulation</topic><topic>Glucose - metabolism</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Ligands</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>multidisciplinary</topic><topic>Necrosis</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>T-Lymphocytes - drug effects</topic><topic>T-Lymphocytes - metabolism</topic><topic>Thioredoxin</topic><topic>Toll-like receptors</topic><topic>Toll-Like Receptors - agonists</topic><topic>Tumor necrosis factor</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Levring, Trine B.</creatorcontrib><creatorcontrib>Kongsbak-Wismann, Martin</creatorcontrib><creatorcontrib>Rode, Anna K. O.</creatorcontrib><creatorcontrib>Al-Jaberi, Fatima A. H.</creatorcontrib><creatorcontrib>Lopez, Daniel V.</creatorcontrib><creatorcontrib>Met, Özcan</creatorcontrib><creatorcontrib>Woetmann, Anders</creatorcontrib><creatorcontrib>Bonefeld, Charlotte M.</creatorcontrib><creatorcontrib>Ødum, Niels</creatorcontrib><creatorcontrib>Geisler, Carsten</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech 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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database (ProQuest)</collection><collection>Biological Science Database</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Levring, Trine B.</au><au>Kongsbak-Wismann, Martin</au><au>Rode, Anna K. O.</au><au>Al-Jaberi, Fatima A. H.</au><au>Lopez, Daniel V.</au><au>Met, Özcan</au><au>Woetmann, Anders</au><au>Bonefeld, Charlotte M.</au><au>Ødum, Niels</au><au>Geisler, Carsten</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tumor necrosis factor induces rapid down-regulation of TXNIP in human T cells</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2019-11-13</date><risdate>2019</risdate><volume>9</volume><issue>1</issue><spage>16725</spage><epage>13</epage><pages>16725-13</pages><artnum>16725</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>In addition to antigen-driven signals, T cells need co-stimulatory signals for robust activation. Several receptors, including members of the tumor necrosis factor receptor superfamily (TNFRSF), can deliver co-stimulatory signals to T cells. Thioredoxin interacting protein (TXNIP) is an important inhibitor of glucose uptake and cell proliferation, but it is unknown how TXNIP is regulated in T cells. The aim of this study was to determine expression levels and regulation of TXNIP in human T cells. We found that naïve T cells express high levels of TXNIP and that treatment of blood samples with TNF results in rapid down-regulation of TXNIP in the T cells. TNF-induced TXNIP down-regulation correlated with increased glucose uptake. Furthermore, we found that density gradient centrifugation (DGC) induced down-regulation of TXNIP. We demonstrate that DGC induced TNF production that paralleled the TXNIP down-regulation. Treatment of blood with toll-like receptor (TLR) ligands induced TNF production and TXNIP down-regulation, suggesting that damage-associated molecular patterns (DAMPs), such as endogenous TLR ligands, released during DGC play a role in DGC-induced TXNIP down-regulation. Finally, we demonstrate that TNF-induced TXNIP down-regulation is dependent on caspase activity and is caused by caspase-mediated cleavage of TXNIP.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>31723203</pmid><doi>10.1038/s41598-019-53234-x</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0003-2707-9313</orcidid><orcidid>https://orcid.org/0000-0002-8472-0771</orcidid><orcidid>https://orcid.org/0000-0003-3135-5624</orcidid><orcidid>https://orcid.org/0000-0002-0523-6229</orcidid><orcidid>https://orcid.org/0000-0002-3496-9333</orcidid><orcidid>https://orcid.org/0000-0002-3008-735X</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2045-2322 |
| ispartof | Scientific reports, 2019-11, Vol.9 (1), p.16725-13, Article 16725 |
| issn | 2045-2322 2045-2322 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6853882 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Springer Nature OA Free Journals; Nature Free; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
| subjects | 13 13/95 631/250/1619/554 631/250/516 82 82/80 Blood Carrier Proteins - antagonists & inhibitors Carrier Proteins - genetics Carrier Proteins - metabolism Caspase Cell activation Cell proliferation Centrifugation Down-Regulation Glucose - metabolism Humanities and Social Sciences Humans Ligands Lymphocytes Lymphocytes T multidisciplinary Necrosis Science Science (multidisciplinary) T-Lymphocytes - drug effects T-Lymphocytes - metabolism Thioredoxin Toll-like receptors Toll-Like Receptors - agonists Tumor necrosis factor Tumor Necrosis Factor-alpha - pharmacology Tumor necrosis factor-TNF |
| title | Tumor necrosis factor induces rapid down-regulation of TXNIP in human T cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-24T05%3A13%3A10IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Tumor%20necrosis%20factor%20induces%20rapid%20down-regulation%20of%20TXNIP%20in%20human%20T%20cells&rft.jtitle=Scientific%20reports&rft.au=Levring,%20Trine%20B.&rft.date=2019-11-13&rft.volume=9&rft.issue=1&rft.spage=16725&rft.epage=13&rft.pages=16725-13&rft.artnum=16725&rft.issn=2045-2322&rft.eissn=2045-2322&rft_id=info:doi/10.1038/s41598-019-53234-x&rft_dat=%3Cproquest_pubme%3E2314558679%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2314315570&rft_id=info:pmid/31723203&rfr_iscdi=true |