JOURNAL ARTICLE

Ca2+/Calmodulin induces translocation of membrane-associated TSC2 to the nucleus where it suppresses CYP24A1 expression.

  • Published In: Bioscience, Biotechnology & Biochemistry, 2023, v. 87, n. 1. P. 45 1 of 3

  • Database: Academic Search Ultimate 2 of 3

  • Authored By: Machiko Kazami; Tomoya Sakamoto; Tsukasa Suzuki; Hirofumi Inoue; Hayato Kato; Ken-Ichi Kobayashi; Tadahiro Tadokoro; Yuji Yamamoto 3 of 3

Abstract

This article investigates the role of calcium/calmodulin (Ca2+/CaM) signaling in regulating the intracellular localization and function of tuberous sclerosis complex 2 (TSC2), a tumor-suppressor protein. The study demonstrates that increased intracellular Ca2+ activates CaM, which induces the translocation of membrane-associated TSC2 to the nucleus in rat brain and HeLa cells. In the nucleus, TSC2 forms a complex with the vitamin D receptor (VDR) and partially suppresses the transcription of CYP24A1, a VDR target gene involved in vitamin D metabolism. These findings suggest that Ca2+/CaM signaling modulates VDR-mediated transcription via TSC2, indicating a novel pathway by which TSC2 may influence cellular processes beyond its established role in mTOR regulation.

Additional Information

  • Source:Bioscience, Biotechnology & Biochemistry. 2023/01, Vol. 87, Issue 1, p45
  • Document Type:Article
  • Subject Area:Health and Medicine
  • Publication Date:2023
  • ISSN:0916-8451
  • DOI:10.1093/bbb/zbac174
  • Accession Number:161134558
  • Copyright Statement:Copyright of Bioscience, Biotechnology & Biochemistry is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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