PIH1D1 interacts with mTOR complex 1 and enhances ribosome RNA transcription. Issue 20 (11th September 2013)

• Record Type: Journal Article
• Authors: Kamano, Yuya; Saeki, Makio; Egusa, Hiroshi; Kakihara, Yoshito; Houry, Walid A.; Yatani, Hirofumi; Kamisaki, Yoshinori
• Is Part Of: FEBS letters. Volume 587:Issue 20(2013)
• Page Start: 3303
• Page End: 3308
• Publication Date: 2013-09-11
• Subjects: Monad -- PIH1D1 -- R2TP -- Breast cancer -- mTOR -- Ribosome; Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular biology -- Periodicals; Biochimie -- Périodiques; Biochemistry; Biophysics; Molecular biology; Periodicals; 572.05
• DOI: 10.1016/j.febslet.2013.09.001
• Languages: English
• ISSNs: 0014-5793

Abstract

Abstract : PIH1D1 is the defining component of the R2TP complex. Recently, R2TP has been reported to stabilize mTOR (mammalian target of rapamycin), an important regulator of cell growth and protein synthesis. Two complexes of mTOR, mTORC1 and mTORC2, have been identified. We demonstrate that immunoprecipitation (IP) of PIH1D1 results in the co‐IP of Raptor (mTORC1 specific), but not Rictor (mTORC2 specific), and that knockdown of PIH1D1 decreases mTORC1 assembly, S6 kinase phosphorylation (indicator of mTORC1 activity), and rRNA transcription without affecting mTORC2 in human breast cancer MCF‐7 cells. In addition, we provide evidence that PIH1D1 is overexpressed in various breast cancer cell lines. These findings collectively suggest that PIH1D1 may have an important role in mTORC1 regulation in breast cancers. Abstract : PIH1D1 interacts with mTOR complex 1. PIH1D1 is overexpressed in various breast cancer cell lines. PIH1D1 enhances rRNA transcription by regulating mTOR complex 1 activity.