{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T17:13:33Z","timestamp":1790356413838,"version":"4.1.0"},"reference-count":53,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2025,1,6]],"date-time":"2025-01-06T00:00:00Z","timestamp":1736121600000},"content-version":"vor","delay-in-days":2228,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>The innate immune system provides a primary line of defense against pathogens. Stimulator of IFN genes (STING), encoded by the TMEM173 gene, is a critical protein involved in IFN-\u03b2 induction in response to infection by different pathogens. In this study, we describe the expression of three different alternative-spliced human (h) TMEM173 mRNAs producing STING truncated isoforms 1, 2, and 3 in addition to the full-length wild-type (wt) hSTING. All of the truncated isoforms lack exon 7 and share the N-terminal transmembrane region with wt hSTING. Overexpression of the three STING truncated isoforms failed to induce IFN-\u03b2, and they acted as selective pathway inhibitors of wt hSTING even in combination with upstream inducer cyclic-di-GMP-AMP synthase. Truncated isoforms alter the stability of wt hSTING, reducing protein t \u00a01\/2 to some extent by the induction of proteasome-dependent degradation. Knocking down expression of truncated isoforms increased production of IFN-\u03b2 by THP1 monocytes in response to intracellular cytosolic DNA or HSV-1 infection. At early stages of infection, viruses like HSV-1 or vesicular stomatitis virus reduced the ratio of full-length wt hSTING\/truncated STING isoforms, suggesting the skewing of alternative splicing of STING toward truncated forms as a tactic to evade antiviral responses. Finally, in silico analysis revealed that the human intron\u2013exon gene architecture of TMEM173 (splice sites included) is preserved in other mammal species, predominantly primates, stressing the relevance of alternative splicing in regulating STING antiviral biology.<\/jats:p>","DOI":"10.4049\/immunohorizons.1800068","type":"journal-article","created":{"date-parts":[[2018,12,11]],"date-time":"2018-12-11T19:55:11Z","timestamp":1544558111000},"page":"363-376","source":"Crossref","is-referenced-by-count":21,"title":["TMEM173 Alternative Spliced Isoforms Modulate Viral Replication through the STING Pathway"],"prefix":"10.1093","volume":"2","author":[{"given":"Estefan\u00eda","family":"Rodr\u00edguez-Garc\u00eda","sequence":"first","affiliation":[{"name":"Gene Therapy and Regulation of Gene Expression Program, Center for Applied Medical Research, University of Navarra, Navarra Institute for Health Research , 31008 Pamplona ,","place":["Spain"]},{"name":"Instituto de Salud Tropical, University of Navarra, Navarra Institute for Health Research , 31008 Pamplona ,","place":["Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cristina","family":"Olag\u00fce","sequence":"additional","affiliation":[{"name":"Gene Therapy and Regulation of Gene Expression Program, Center for Applied Medical Research, University of Navarra, Navarra Institute for Health Research , 31008 Pamplona ,","place":["Spain"]},{"name":"Instituto de Salud Tropical, University of Navarra, Navarra Institute for Health Research , 31008 Pamplona ,","place":["Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sergio","family":"R\u00edus-Rocabert","sequence":"additional","affiliation":[{"name":"Microbiology Section, Department of Pharmaceutical and Health Science, Faculty of Pharmacy, University San Pablo\u2013CEU, CEU Universities, Campus Montepr\u00edncipe , 28668 Madrid ,","place":["Spain"]},{"name":"Institute of Applied Molecular Medicine, University San Pablo\u2013CEU, CEU Universities, Campus Montepr\u00edncipe , 28668 Madrid ,","place":["Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7015-4844","authenticated-orcid":false,"given":"Roberto","family":"Ferrero","sequence":"additional","affiliation":[{"name":"Gene Therapy and Regulation of Gene Expression Program, Center for Applied Medical Research, University of Navarra, Navarra Institute for Health Research , 31008 Pamplona ,","place":["Spain"]},{"name":"Instituto de Salud Tropical, University of Navarra, Navarra Institute for Health Research , 31008 Pamplona ,","place":["Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carlos","family":"Llorens","sequence":"additional","affiliation":[{"name":"Biotechvana , 46980 Valencia 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,","place":["Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jes\u00fas","family":"Prieto","sequence":"additional","affiliation":[{"name":"Gene Therapy and Regulation of Gene Expression Program, Center for Applied Medical Research, University of Navarra, Navarra Institute for Health Research , 31008 Pamplona ,","place":["Spain"]},{"name":"Instituto de Salud Tropical, University of Navarra, Navarra Institute for Health Research , 31008 Pamplona ,","place":["Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1600-4562","authenticated-orcid":false,"given":"Gloria","family":"Gonz\u00e1lez-Aseguinolaza","sequence":"additional","affiliation":[{"name":"Gene Therapy and Regulation of Gene Expression Program, Center for Applied Medical Research, University of Navarra, Navarra Institute for Health Research , 31008 Pamplona ,","place":["Spain"]},{"name":"Instituto de Salud Tropical, University of Navarra, Navarra 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