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- W4308184067 abstract "ABSTRACT 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." @default.
- W4308184067 created "2022-11-09" @default.
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- W4308184067 date "2022-11-04" @default.
- W4308184067 modified "2023-10-16" @default.
- W4308184067 title "Ca2+/Calmodulin induces translocation of membrane-associated TSC2 to the nucleus where it suppresses <i>CYP24A1</i> expression" @default.
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- W4308184067 doi "https://doi.org/10.1093/bbb/zbac174" @default.
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