RagA, an mTORC1 activator, interacts with a hedgehog signaling protein, WDR35/IFT121

Takeshi Sekiguchi, Nobuaki Furuno, Takashi Ishii, Eiji Hirose, Fumiko Sekiguchi, Yonggang Wang, Hideki Kobayashi

研究成果: ジャーナルへの寄稿学術誌査読

3 被引用数 (Scopus)

抄録

Small Ras-like GTPases act as molecular switches for various signal transduction pathways. RagA, RagB/RagC and RagD are small Ras-like GTPases that play regulatory roles in mTORC1. Lack of proper activation of mTORC1 can lead to diseases, such as cancer and diabetes. In this study, we found an interaction between RagA and WDR35. Mutations of WDR35 may cause genetic diseases including Sensenbrenner syndrome. WDR35 seems to be a hedgehog signaling protein with a possible ciliary function and a possible upstream regulator of RagA. RagB is a homologue of RagA and is also associated with WDR35. WDR35 is present in the endoplasmic reticulum, but usually not in lysosomes, where Rag family proteins act as an mTORC1 switch. Over-expression of WDR35 results in decreased phosphorylation of ribosome S6 protein in a RagA-, RagB- and RagC-dependent manner. Thus, WDR35 is associated with RagA, RagB and RagC and might negatively influence mTORC1 activity.

本文言語英語
ページ(範囲)151-161
ページ数11
ジャーナルGenes to Cells
24
2
DOI
出版ステータス出版済み - 2月 2019
外部発表はい

!!!All Science Journal Classification (ASJC) codes

  • 遺伝学
  • 細胞生物学

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