TBCK Influences Cell Proliferation, Cell Size and mTOR Signaling Pathway

作者：Yueli Liu, Xiaoyi Yan, Tianhua Zhou · 发表于：PLoS ONE · 年份：2013 · DOI：10.1371/journal.pone.0071349 · 被引用次数：62 · 研究领域：PI3K/AKT/mTOR signaling in cancer、Protein Kinase Regulation and GTPase Signaling、Coagulation, Bradykinin, Polyphosphates, and Angioedema

Mammalian target of rapamycin (mTOR) is a central regulator for both cell proliferation and cell growth; however, little is known about the regulation of mTOR expression at the transcriptional level. Here, we provide evidences that a conserved human protein TBCK (TBC1 domain containing kinase) is involved in the regulation of mTOR signaling pathway. Depletion of TBCK significantly inhibits cell proliferation, reduces cell size, and disrupts the organization of actin, but not microtubule. Knockdown of TBCK induces a significant decrease in the protein levels of components of mTOR complex (mTORC), and suppresses the activity of mTOR signaling, but not MAPK or PDK1/Akt pathway. Further results show that TBCK influences the expression of mTORC components at the transcriptional level. Thus, these data suggest that TBCK may play an important role in cell proliferation, cell growth and actin organization possibly by modulating mTOR pathway.