{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T10:47:34Z","timestamp":1792406854678,"version":"4.4.0"},"reference-count":45,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T00:00:00Z","timestamp":1792368000000},"content-version":"vor","delay-in-days":18,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T00:00:00Z","timestamp":1790812800000},"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":["82270495"],"award-info":[{"award-number":["82270495"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["analyticalsciencejournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cell Biochemistry &amp;amp; Function"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>PDE4DIP\/Myomegalin was originally identified as a Golgi\u2010 and centrosome\u2010associated protein that interacts with phosphodiesterase 4D, but subsequent work has placed it within a broader network of organelle\u2010associated signaling and cytoskeletal regulation. This review examines PDE4DIP\/Myomegalin as a coiled\u2010coil\u2010rich scaffold linking compartmentalized cyclic adenosine monophosphate (cAMP)\/protein kinase A (PKA) signaling, Golgi\u2013centrosome organization, microtubule architecture, and disease\u2010associated pathway remodeling. At the centrosome, long PDE4D\u2010binding myomegalin forms retain PDE4D3 and restrict local PKA activity, thereby influencing Hedgehog signaling. At the Golgi, AKAP9\/AKAP450 provides a major scaffold, while selected myomegalin forms support Golgi\u2010derived microtubule organization and endoplasmic reticulum\u2013Golgi trafficking. In KRAS\u2010mutant colorectal cancer models, PDE4DIP promotes tumor growth and MEK inhibitor resistance through Golgi\u2010associated NF1\/RAS pathway remodeling. In non\u2010small cell lung cancer, PDE4DIP cooperates with AKAP9 to maintain Golgi localization and stability of PKA regulatory subunit II alpha; PDE4DIP loss activates PKA\/cAMP response element\u2010binding protein signaling and suppresses tumor growth. Cardiovascular studies link myomegalin isoform 4 to sarcomeric PKA signaling, co\u2010occurring PDE4DIP and DES variants to conduction phenotypes, and PDE4DIP dysregulation to left ventricular noncompaction\u2010associated cellular changes, although the evidence remains context dependent. Neurological and retinal disease associations remain largely exploratory. Recent work links a PDE4DIP\u2013AKAP9 interaction to cytoskeletal integrity and RAS\u2013ERK\/AKT signaling in podocyte injury. Overall, PDE4DIP\/Myomegalin is best understood as an organelle\u2010associated organizer whose effects depend on the experimentally reported form, binding partners, and subcellular address rather than on a single linear pathway.<\/jats:p>","DOI":"10.1002\/cbf.70325","type":"journal-article","created":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T10:20:07Z","timestamp":1792405207000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["PDE4DIP\/Myomegalin as a Golgi\u2013Centrosome Scaffold in Compartmentalized Signaling, Microtubule Organization, and Disease\u2010Associated Pathway Remodeling"],"prefix":"10.1002","volume":"44","author":[{"given":"Cong","family":"Wang","sequence":"first","affiliation":[{"name":"Department of General Surgery, Xuanwu Hospital Capital Medical University Beijing Beijing China"},{"name":"National Clinical Research Center for Geriatric Diseases Beijing Beijing 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