{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T05:56:01Z","timestamp":1790574961616,"version":"4.1.0"},"reference-count":52,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T00:00:00Z","timestamp":1789084800000},"content-version":"vor","delay-in-days":10,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T00:00:00Z","timestamp":1788220800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82273539"],"award-info":[{"award-number":["82273539"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Psoriasis is a chronic and recurrent inflammatory dermatosis characterized by dysregulated keratinocyte proliferation. Calcium\u2010binding protein 39 (CAB39), a critical regulatory scaffold for Sterile 20 kinase, has been implicated in multiple diseases, but its role and regulatory mechanisms in psoriasis remain unclear. Here, we found that CAB39 was significantly upregulated in psoriatic lesions, and\n                    <jats:italic>CAB39<\/jats:italic>\n                    knockdown inhibited keratinocyte proliferation and attenuated psoriasis progression. Further investigations revealed that CAB39 crotonylation at lysine 196 was reduced in psoriatic lesions. Functional analyses in normal human epidermal keratinocytes (NHEKs) showed that the crotonylation\u2010deficient CAB39 K196A mutant significantly promoted keratinocyte hyperproliferation and glycolytic remodeling. Dysregulation of modifying enzymes, including downregulated CBP and upregulated HDAC2\/3, drives CAB39 K196 decrotonylation in psoriasis. Mechanistically, CAB39 K196 decrotonylation weakens its binding affinity to STRAD (STE20\u2010related adaptor), disrupts the stability of the CAB39\u2010STRAD\u2010LKB1 (liver kinase B1) complex, and inhibits the LKB1\/AMPK signaling pathway. Concurrently, decrotonylated CAB39 promotes phosphatidic acid (PA, a lipid second messenger) synthesis, activating the pro\u2010proliferative PA\/MAPK\/mTOR signaling cascade. Our findings uncover a novel pathogenic mechanism in psoriasis, wherein CAB39 K196 decrotonylation drives keratinocyte dysfunction, and expand our understanding of non\u2010histone crotonylation in inflammatory skin diseases. Importantly, targeting the CBP\/HDAC2\/3\u2010CAB39 crotonylation axis may represent a potential therapeutic strategy for psoriasis.\n                  <\/jats:p>","DOI":"10.1002\/jcp.70224","type":"journal-article","created":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T09:35:58Z","timestamp":1789119358000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["CAB39 K196 Decrotonylation Drives Psoriasis Pathogenesis by Modulating Keratinocyte Proliferation and Glycolysis"],"prefix":"10.1002","volume":"241","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3788-7584","authenticated-orcid":false,"given":"Huifang","family":"Liang","sequence":"first","affiliation":[{"name":"ShanXi Key Laboratory of Stem Cells for Immunological Dermatosis, State Key Breeding Laboratory of Stem Cells for Immunological Dermatosis Institute of Dermatology, Taiyuan City Central Hospital Taiyuan 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