{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T06:04:11Z","timestamp":1790229851082,"version":"4.1.0"},"reference-count":75,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T00:00:00Z","timestamp":1790208000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Stimulator of interferon genes (STING) is a key player in innate immunity, and its dysregulation has been implicated in autoimmune and inflammatory diseases. The activation of STING is regulated by multiple factors, including post-translational modifications (PTMs), but the regulatory network of these PTMs remains incompletely characterized. Here, we report that vascular non-inflammatory molecule-1 (Vanin-1) facilitates STING activation and provide evidence supporting S-cysteaminylation as a previously unrecognized modification of STING. Mechanistically, Vanin-1 hydrolyzes pantetheine to pantothenic acid (vitamin B5) and cysteamine, an aminothiol that promotes S-cysteaminylation of STING at three conserved cysteine residues within the transmembrane domain and potentiates agonist-induced STING activation without directly activating STING. Genetic and pharmacological inhibition of Vanin-1 attenuated STING signaling induced by STING agonists and ameliorated DSS-induced colitis\n                    <jats:italic>in vivo<\/jats:italic>\n                    . Together, our findings reveal a novel regulatory role for Vanin-1 in the cGAS-STING pathway and suggest that Vanin-1 may represent a potential therapeutic target for inflammatory diseases characterized by aberrant cGAS-STING activation.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1921134","type":"journal-article","created":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T05:41:32Z","timestamp":1790228492000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Pantetheinase Vanin-1 potentiates agonist-induced STING activation via S-cysteaminylation"],"prefix":"10.3389","volume":"17","author":[{"given":"Ximing","family":"Liao","sequence":"first","affiliation":[{"name":"State Key Laboratory of Chemical Oncogenomics, Peking University Shenzhen Graduate School","place":["Shenzhen, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiamiao","family":"Fu","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Chemical Oncogenomics, Peking University Shenzhen Graduate School","place":["Shenzhen, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chuchu","family":"Xie","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Chemical Oncogenomics, Peking University Shenzhen Graduate School","place":["Shenzhen, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Siyu","family":"Liu","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Chemical Oncogenomics, Peking University Shenzhen Graduate School","place":["Shenzhen, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoquan","family":"Wang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Chemical Oncogenomics, Peking University Shenzhen Graduate School","place":["Shenzhen, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Minqiang","family":"Hu","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Chemical Oncogenomics, Peking University Shenzhen Graduate School","place":["Shenzhen, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junmin","family":"Quan","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Chemical Oncogenomics, Peking University Shenzhen Graduate School","place":["Shenzhen, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,24]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/nature07317","article-title":"Sting is an endoplasmic reticulum adaptor that facilitates innate immune 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