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PIH1D1 interacts with mTOR complex 1 and enhances ribosome RNA transcription
Author(s) -
Kamano Yuya,
Saeki Makio,
Egusa Hiroshi,
Kakihara Yoshito,
Houry Walid A.,
Yatani Hirofumi,
Kamisaki Yoshinori
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.09.001
Subject(s) - mtorc2 , mtorc1 , pi3k/akt/mtor pathway , microbiology and biotechnology , transcription (linguistics) , cancer research , immunoprecipitation , biology , transcription factor , gene knockdown , phosphorylation , ribosome , mechanistic target of rapamycin , p70 s6 kinase 1 , chemistry , rna , signal transduction , genetics , gene , linguistics , philosophy
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.