دورية أكاديمية
أعرض في EDS

PKCμ promotes keratinocyte cell migration through Cx43 phosphorylation-mediated suppression of intercellular communication.

التفاصيل البيبلوغرافية
العنوان: PKCμ promotes keratinocyte cell migration through Cx43 phosphorylation-mediated suppression of intercellular communication.
المؤلفون: Pun R; Biomedical Sciences Department, School of Medicine, Creighton University, Omaha, NE 68178, USA., Cavanaugh AM; Department of Biology, College of Arts and Sciences, Creighton University, Omaha, NE 68178, USA., Aldrich E; Biomedical Sciences Department, School of Medicine, Creighton University, Omaha, NE 68178, USA., Tran O; Biomedical Sciences Department, School of Medicine, Creighton University, Omaha, NE 68178, USA., Rudd JC; Biomedical Sciences Department, School of Medicine, Creighton University, Omaha, NE 68178, USA., Hansen LA; Biomedical Sciences Department, School of Medicine, Creighton University, Omaha, NE 68178, USA., North BJ; Biomedical Sciences Department, School of Medicine, Creighton University, Omaha, NE 68178, USA.
المصدر: IScience [iScience] 2024 Jan 29; Vol. 27 (3), pp. 109033. Date of Electronic Publication: 2024 Jan 29 (Print Publication: 2024).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 101724038 Publication Model: eCollection Cited Medium: Internet ISSN: 2589-0042 (Electronic) Linking ISSN: 25890042 NLM ISO Abbreviation: iScience Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: [Cambridge, MA] : Cell Press, [2018]-
مستخلص: Downregulation of intercellular communication through suppression of gap junctional conductance is necessary during wound healing. Connexin 43 (Cx43), a prominent gap junction protein in skin, is downregulated following wounding to restrict communication between keratinocytes. Previous studies found that PKCμ, a novel PKC isozyme, regulates efficient cutaneous wound healing. However, the molecular mechanism by which PKCμ regulates wound healing remains unknown. We have identified that PKCμ suppresses intercellular communication and enhances cell migration in an in vitro wound healing model by regulating Cx43 containing gap junctions. PKCμ can directly interact with and phosphorylate Cx43 at S368, which leads to Cx43 internalization and downregulation. Finally, utilizing phosphomimetic and non-phosphorylatable S368 substitutions and gap junction inhibitors, we confirmed that PKCμ regulates intercellular communication and in vitro wound healing by controlling Cx43-S368 phosphorylation. These results define PKCμ as a critical regulator of Cx43 phosphorylation to control cell migration and wound healing in keratinocytes.
Competing Interests: The authors declare no competing interests.
(© 2024 The Author(s).)
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فهرسة مساهمة: Keywords: Biological sciences; Cell biology; Molecular biology; Molecular interaction
تواريخ الأحداث: Date Created: 20240220 Latest Revision: 20240221
رمز التحديث: 20240221
مُعرف محوري في PubMed: PMC10875573
DOI: 10.1016/j.isci.2024.109033
PMID: 38375220
قاعدة البيانات: MEDLINE
الوصف
تدمد:2589-0042
DOI:10.1016/j.isci.2024.109033