| Autor: |
Machiko Kazami, Tomoya Sakamoto, Tsukasa Suzuki, Hirofumi Inoue, Hayato Kato, Ken-Ichi Kobayashi, Tadahiro Tadokoro, Yuji Yamamoto |
| Předmět: |
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| Zdroj: |
Bioscience, Biotechnology & Biochemistry; Jan2023, Vol. 87 Issue 1, p45-53, 9p |
| Abstrakt: |
Tuberous sclerosis complex 2 (TSC2) is a tumor-suppressor protein. A loss of TSC2 function induces hyperactivation of mechanistic target of rapamycin (mTOR). The C-terminal region of TSC2 contains a calmodulin (CaM) binding region and the CaM-TSC2 interaction contributes to proper mTOR activity. However, other downstream signaling pathways/effectors activated by the CaM-TSC2 complex have not been fully elucidated. In this study, we found that activation of Ca2+/CaM signaling resulted in the translocation of membrane-associated TSC2 to the nucleus and suppressed the transcriptional activity of the vitamin D receptor (VDR). TSC2 was released from the membrane in an activated CaM-dependent state in rat brain and HeLa cells. It subsequently formed a transcriptional complex to partially suppress the transcription of CYP24A1, a well-known VDR target gene. These data suggest, in part, that TSC2 attenuates VDR-associated transcriptional regulation via Ca2+/CaM signaling. [ABSTRACT FROM AUTHOR] |
| Databáze: |
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