{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,15]],"date-time":"2026-08-15T14:32:01Z","timestamp":1786804321927,"version":"build-2736575974"},"reference-count":44,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"4","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Adv."],"published-print":{"date-parts":[[2025,1,24]]},"abstract":"<jats:p>\n            S-Palmitoylation is a reversible post-translational modification involving saturated fatty acid palmitate-to-cysteine linkage in the protein, which guides many aspects of macrophage physiology in health and disease. However, the precise role and underlying mechanisms of palmitoylation in\n            <jats:italic>Mycobacterium tuberculosis<\/jats:italic>\n            infection of macrophages remain elusive. Here, we found that\n            <jats:italic>M. tuberculosis<\/jats:italic>\n            infection induced the expression of zinc-finger DHHC domain\u2013type palmitoyl-transferases (ZDHHCs), particularly ZDHHC2, in mouse macrophages. Furthermore, ZDHHC2 deficiency in mouse macrophages impaired the immunity against\n            <jats:italic>M. tuberculosis<\/jats:italic>\n            and reduced the production of various proinflammatory cytokines. Mechanistic studies revealed the involvement of ZDHHC2 in mediating the palmitoylation of B-RAF and C-RAF, affecting their autophagic degradation and stabilizing protein levels. The increased abundance of B-RAF and C-RAF subsequently increases the activity of the extracellular signal\u2013regulated kinase (ERK) signaling pathway, affecting the survival of\n            <jats:italic>M. tuberculosis<\/jats:italic>\n            within macrophages. These findings suggest that ZDHHC2 is a potential target for treating tuberculosis.\n          <\/jats:p>","DOI":"10.1126\/sciadv.adq7706","type":"journal-article","created":{"date-parts":[[2025,1,24]],"date-time":"2025-01-24T18:58:38Z","timestamp":1737745118000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":12,"title":["ZDHHC2 promoted antimycobacterial responses by selective autophagic degradation of B-RAF and C-RAF in macrophages"],"prefix":"10.1126","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1195-809X","authenticated-orcid":true,"given":"Junli","family":"Sheng","sequence":"first","affiliation":[{"name":"Institute of Molecular Immunology, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China."},{"name":"Guangdong Provincial Key Laboratory of Allergy &amp; Clinical Immunology, The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, 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