A direct linkage between the phosphoinositide 3-kinase-AKT signaling pathway and the mammalian target of rapamycin in mitogen-stimulated and transformed cells.

By A. Sekulic, Christine C. Hudson, J. Homme, Peng Yin, D. Otterness, L. Karnitz, R. Abraham. Cancer Research, 2000

787 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/4ab6203dcb36410c26914c3eafc6d07dcd28f50b

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Citations in the corpus

Upstream and downstream of mTOR. (2004, background): “mTOR also contains a putative negative regulatory domain (NRD) between the catalytic and FATC domains (Fig. 1; Sekulic et al. 2000).”
PI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer (2023, background): “consequently, Rheb turns into GTP loaded, leading to activation of mTORC1, recruited by Rag proteins [150] (Fig.”
Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake. (2002, background): “The kinase activity of mTOR may be modulated by Akt activity (Scott et al., 1998; Sekulic et al., 2000), and several studies suggest that the transforming effects of Akt involve stimulation of mTOR (Aoki et al.”
Mammalian cell size is controlled by mTOR and its downstream targets S6K1 and 4EBP1/eIF4E. (2002, background): “mTOR may also respond to mitogenic signals (Scott et al. 1998; Sekulic et al. 2000; Fang et al. 2001).”
Insulin receptor isoforms and insulin receptor/insulin-like growth factor receptor hybrids in physiology and disease. (2009, background): “mTOR is regulated by insulin/IGFs and other growth factors through the PI3K– Akt pathway (281) and is abnormally activated in most cancer cells.”
Regulation of cellular growth by the Drosophila target of rapamycin dTOR. (2000, background): “Akt can stimulate the kinase activity of mTOR immunoprecipitates and can phosphorylate mTOR in vitro (Scott et al. 1998; Navé et al. 1999; Sekulic et al. 2000).”
Defining the role of mTOR in cancer. (2007, background): “Other subunits of mTORC1 are also phosphorylated (including mTOR at S2448 [Sekulic et al., 2000], which is commonly used as a biomarker of mTOR activation), but the functional significance of these modifications is unclear.”
Akt/protein kinase B is constitutively active in non-small cell lung cancer cells and promotes cellular survival and resistance to chemotherapy and radiation. (2001, background): “(LY294002 may also have nonspecific effects; but only inhibition of the mammalian target of rapamycin, an Akt/PKB substrate (74), by LY294002 has been reported at doses used in these experiments (75).”
TSC2 mediates cellular energy response to control cell growth and survival. (2003, background): “correlate with mTOR activity (Nave et al., 1999; Scott et al., 1998; Sekulic et al., 2000), was also inhibited by 25 We also performed coimmunoprecipitation studies between endogenous AMPK and overexpressed TSC2 mM 2DG (Figure 1C).”
Activation of the PI3K/Akt pathway and chemotherapeutic resistance. (2002, background): “Initial in vitro studies with rapamycin demonstrated the sensitivity of several tumor cell lines to the growth inhibition and apoptotic effects of rapamycin (Hosoi et al., 1999; Sekulic et al., 2000; Seufferlein and Rozengurt, 1996).”