IndraLab
Statements
MTOR is active.
3
9
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1
"Importantly, phosphorylation of mTOR by S6K1 occurs at threonine 2446/serine 2448. This region has been shown previously to be part of a regulatory repressor domain. These sites are also constitutively phosphorylated in the breast cancer cell line MCF7 carrying an amplification of the S6K1 geneit has been proposed that other inputs, in addition to phosphorylation of Thr-2446/Ser-2448 by S6K1, are part of the mechanism involved in inhibiting this repressor domain"
"Importantly, phosphorylation of mTOR by S6K1 occurs at threonine 2446/serine 2448. This region has been shown previously to be part of a regulatory repressor domain. These sites are also constitutively phosphorylated in the breast cancer cell line MCF7 carrying an amplification of the S6K1 geneit has been proposed that other inputs, in addition to phosphorylation of Thr-2446/Ser-2448 by S6K1, are part of the mechanism involved in inhibiting this repressor domain"
"We report here the identification of a FRAP autophosphorylation site. This site, Ser-2481, is located in a hydrophobic region near the conserved carboxyl-terminal FRAP tail. We demonstrate that the COOH-terminal tail is required for FRAP kinase activity and for signaling to the translational regulator p70(s6k) (ribosomal subunit S6 kinase)."
MTOR is kinase-active.
3
2
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"We first studied the effect of 12 h exposure to T3 on S2448 phosphorylation of mTOR to match the exposure time for Northern blot analysis (Fig. 1A). As shown in Fig. 1B, an increase in S2448 phosphorylation was detected after 12 h exposure to T3....The phosphorylation is associated with a marked increase in T389 phosphorylation of p70S6K. These results demonstrate T3-dependent phosphorylation of S2448 activates mTOR kinase."
"We first studied the effect of 12 h exposure to T3 on S2448 phosphorylation of mTOR to match the exposure time for Northern blot analysis (Fig. 1A). As shown in Fig. 1B, an increase in S2448 phosphorylation was detected after 12 h exposure to T3....The phosphorylation is associated with a marked increase in T389 phosphorylation of p70S6K. These results demonstrate T3-dependent phosphorylation of S2448 activates mTOR kinase."
MTOR is inactive.
5
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"Although AKT phosphorylated mTOR at two COOH-terminal sites (Thr2446 and Ser2448) in vitro, Ser2448 was the major phosphorylation site in insulin-stimulated or -activated AKT-expressing human embryonic kidney cells. Transient transfection assays with mTOR mutants bearing Ala substitutions at Ser2448 and/or Thr2446 indicated that AKT-dependent mTOR phosphorylation was not essential for either PHAS-I phosphorylation or p70S6K activation in HEK cells."
"AKT phosphorylated mTOR at two COOH-terminal sites (Thr2446 and Ser2448) in vitro, Ser2448 was the major phosphorylation site in insulin-stimulated or -activated AKT-expressing human embryonic kidney cells. These results demonstrate that mTOR is a direct target of the PI3K-AKT signaling pathway in mitogen-stimulated cells, and that the identified AKT phosphorylation sites are nested within a repressor domain that negatively regulates the catalytic activity of mTOR."