◀ Back to MTOR

ANXA6 — MTOR

Text-mined interactions from Literome

Zhang et al., Cancer Biol Ther 2009 : PIM1 protein kinase overexpression reduced the association of PRAS40 with mTOR, and increased the mTOR directed phosphorylation of 4EBP1 and p70S6Kinase
Shen et al., International journal of clinical and experimental pathology 2010 (Carcinoma, Endometrioid...) : mTORC1 and mTORC2 phosphorylatively regulate their respective downstream effectors p70S6K/4EBP1 , and Akt ... mTORC1 and mTORC2 phosphorylatively regulate their respective downstream effectors p70S6K/4EBP1 , and Akt
Kuehn et al., J Biol Chem 2011 : In mouse bone marrow derived mast cells, PGE ( 2 ) was found to induce activation of mTORC1 ( mTOR complexed to raptor ) as indicated by increased p70S6K and 4E-BP1 phosphorylation, and activation of mTORC2 ( mTOR complexed to rictor ), as indicated by increased phosphorylation of AKT at position Ser ( 473 )
Han et al., Cancer Res 2006 (Carcinoma, Non-Small-Cell Lung...) : Rapamycin, an inhibitor of mTOR , blocked the fibronectin induced phosphorylation of p70S6K and 4E-BP1
Sini et al., Autophagy 2010 (Neoplasms) : mTORC1 activates p70S6K , which in turn phosphorylates the ribosomal protein S6 and 4E-BP1, both involved in protein translation
Shao et al., Cancer Res 2004 (Cell Transformation, Neoplastic...) : p70 ribosomal protein S6 kinase activity was induced by K-Ras in a PI3K- and mTOR dependent manner
Feng et al., J Biol Chem 2000 : We now demonstrate that SCF activates phosphoinositide 3-kinase (PI3-K) and p70 S6 kinase (p70S6K) and that rapamycin, a FRAP/mammalian target of rapamycin dependent inhibitor of p70S6K , completely inhibited bromodeoxyuridine incorporation induced by SCF in primary cultures of spermatogonia
Huang et al., Cancer Res 2002 : Ultraviolet induced phosphorylation of p70 ( S6K ) at Thr ( 389 ) and Thr ( 421 ) /Ser ( 424 ) involves hydrogen peroxide and mammalian target of rapamycin but not Akt and atypical protein kinase C
Gonzalez-Garcia et al., J Biol Chem 2002 : Formation of this complex is not required for activation of a FRAP independent form of p70S6K, however, underscoring the role of p85 in regulating FRAP dependent p70S6K activation
Samadi et al., Surgery 2012 (Thyroid Neoplasms) : Unique from other targeted therapies, withanolides suppressed RET and Akt phosphorylation and protein expression ( in a concentration- and time dependent manner ) as well as mTOR activity and translational activity of 4E-BP1 and protein synthesis mediated by p70S6kinase activation at IC ( 50 ) concentrations
Galbaugh et al., BMC cell biology 2006 : EGF induced activation of Akt results in mTOR dependent p70S6 kinase phosphorylation and inhibition of HC11 cell lactogenic differentiation
Dennis et al., J Biol Chem 2013 : Together, these findings support the conclusion that, in the absence of 4E-BP proteins, mTORC1 mediated phosphorylation of p70S6K1 is elevated by a reduction in competition between the two substrates for interaction with raptor
Sekulić et al., Cancer Res 2000 : 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
El-Chaâr et al., International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity 2004 : Mammalian target of rapamycin (mTOR) is a PKB substrate, and regulates p70 S6 kinase (p70 S6K)
Gu et al., Leukemia 2008 (Cell Transformation, Neoplastic) : The mTOR inhibitor rapamycin suppressed activation of p70S6K in BaF3/NPM-ALK cells and reversed GC resistance by synergistically inhibiting mTOR signaling pathway, enhancing cell cycle arrest at G(1) phase and promoting apoptotic cell death
Medici et al., PloS one 2012 (Hemangioma) : mTOR activates p70S6K , which controls translation of mRNA to generate proteins such as hypoxia inducible factor-1 (HIF-1)
Wang et al., Mol Cell Biol 2007 (Neoplasms) : These results indicate that mTOR inhibitor induced eIF4E phosphorylation is secondary to mTOR/raptor inhibition and independent of p70S6K
Gafford et al., Neuroscience 2011 : Additionally we showed that p70s6K was activated after retrieval of a previously stored fear memory, and inhibition of mTOR by DH infusion of RAP blocked the reconsolidation of contextual fear memory
Rhoads et al., Am J Physiol Gastrointest Liver Physiol 2006 : We found that 1 ) protein synthesis is required for intestinal cell migration, 2 ) mTOR/p70 ( s6k ) pathway inhibitors ( rapamycin, wortmannin, and intracellular Ca ( 2+ ) chelation ) inhibit cell migration, 3 ) ARG activates migration and mTOR/p70 ( s6k ) ( but not ERK-2 ) in migrating enterocytes, and 4 ) immunocytochemistry reveals abundant p70 ( s6k ) staining in cytoplasm, whereas phospho-p70 ( s6k ) is virtually all intranuclear in resting cells but redistributes to the periphery on activation by ARG
Gu et al., Cell Signal 2013 (Colonic Neoplasms) : Similarly, inhibition of mTOR blocked p70S6K and PAK1 phosphorylation and actin remodeling
Ciechomska et al., Oncogene 2013 (Brain Neoplasms...) : Decrease of phosphorylation of 4E-BP1, p70S6K1 and its downstream target S6 ribosomal protein demonstrate inhibition of mTOR signaling by CsA
Li et al., Am J Physiol Cell Physiol 2011 (MAP Kinase Signaling System) : Here, we demonstrate that the inhibition of mTORC1 by rapamycin ( mTORC1 inhibitor ), torin1 ( both mTORC1 and mTORC2 inhibitor ) or short hairpin RNA mediated knockdown of mTOR, regulatory associated protein of mTOR ( RAPTOR ), and p70 S6 kinase (p70S6K) increased basal NT release via upregulating NT gene expression in BON cells
Hirata et al., Brain Res 2003 (Brain Neoplasms...) : Rapamycin, a specific inhibitor of p70S6K activation by the mammalian target of rapamycin , completely prevents GDNF induced proliferation and activation of p70S6K
Argadine et al., Am J Physiol Cell Physiol 2011 : Phosphorylation of their downstream effector mTOR ( Ser2481 ) did not change at any time point after DNV, and phosphorylated p70S6K and eIF4E binding protein 1 ( 4EBP1 ) increased only by DNV-5D
Avila-Flores et al., J Biol Chem 2005 (Anoxia) : We found that overexpression of the DGKzeta, but not of the alpha isoform, in serum deprived HEK293 cells induced mTOR dependent phosphorylation of p70S6 kinase (p70S6K)
Wu et al., J Biol Chem 2004 : Insulin induced phosphorylation of p70S6K and mTOR was prevented by the mTOR inhibitor, rapamycin
Kim et al., Am J Physiol Endocrinol Metab 2012 : An inhibitor of mTOR , rapamycin, attenuated the ANG II-stimulated phosphorylation of p70S6K and phosphorylation of IRS-1 ( Ser ( 636/639 ) ) and blocked the ability of ANG II to impair insulin stimulated phosphorylation of eNOS, nitric oxide production, and mesenteric-arteriole vasodilation
Le et al., Oncogene 2003 : Inhibitors of mTOR , PI3K, and Ca ( ++ ) impair p70S6K activity, whereas inhibitors of JNK and PKC stimulate p70S6K activity
Faghiri et al., Exp Eye Res 2010 : Inhibition of PI3K or mTOR/p70S6K by wortmannin and rapamycin, respectively, increased apoptosis and inhibited phosphorylation of Akt and p70S6K induced by single-dose oxidative stress
Weinstein et al., J Leukoc Biol 2000 : Inhibitors of PI 3-kinase or the mammalian target of rapamycin (mTOR) fully blocked p70 S6 kinase activation, implying that this kinase is controlled by PI 3-kinase and mTOR
Halayko et al., Am J Respir Cell Mol Biol 2004 (Asthma...) : These studies provide primary evidence that PI(3) kinase and mTOR activate p70S6K in airway myocytes leading to the accumulation of contractile apparatus proteins, differentiation, and growth of large, elongated contractile phenotype airway smooth muscle cells
Brenneisen et al., J Biol Chem 2000 : The FRAP kinase inhibitor rapamycin and the DNA repair inhibitor aphidicolin significantly suppressed the UVB mediated increase in p70 ribosomal S6 kinase activity by 50-65 % and MMP-1 and MMP-3 protein levels by 34-68 % and 42-88 % compared with UVB irradiated fibroblasts
Tang et al., J Biochem Mol Biol 2006 : Furthermore, we found that the overexpression of LPAAT-theta can induce mTOR dependent p70S6K phosphorylation on Thr389 and 4EBP1 phosphorylation on Ser65 in HEK293T cells
Marzec et al., PloS one 2011 (Lymphoma, T-Cell, Cutaneous) : mTORC1 activates p70S6kinase 1 (p70S6K1) and inhibits 4E-binding protein 1 (4E-BP1)
Sarker et al., Oncogene 2004 : Rapamycin, a specific inhibitor of FRAP/mTOR ( the upstream kinase of p70S6K ), also blocked p70S6K activation, indicating the involvement of FRAP/mTOR activation
Murugan et al., J Biol Chem 2013 (Cell Transformation, Neoplastic...) : Stable expression of the two mTOR mutants in NIH3T3 cells strongly activated mTOR/p70S6K signaling, induced cell transformation and invasion, and remarkably, caused rapid tumor formation and growth in athymic nude mice after subcutaneous inoculation of the transfected cells
Hartley et al., J Cell Biochem 2002 : While the role of mTOR in the phosphorylation of IRS-1 appears to proceed primarily through the regulation of PP2A, we also provide evidence that the regulation of p70S6 kinase phosphorylation requires the direct activity of mTOR
Syed et al., Photochem Photobiol 2006 : mTOR , structurally related to PI3K, is involved in the regulation of p70S6K , which in turn phosphorylates the S6 protein of the 40S ribosomal subunit
Rosner et al., Amino Acids 2010 : So far, the role of p70S6K mediated mTOR S2448 phosphorylation has not been investigated in detail
Lee et al., J Biol Chem 2005 : We also show that insulin stimulated the phosphorylation of 4E-binding protein 1 (4E-BP1) and p70S6 kinase (p70S6K) in a mTOR dependent manner
Gibbons et al., Semin Oncol 2009 (Neoplasms) : Activated mTORC1 regulates protein synthesis by directly phosphorylating 4E-binding protein 1 (4E-BP1) and p70S6K ( S6K ), translation initiation factors that are important to cap dependent mRNA translation, which increases the level of many proteins that are needed for cell cycle progression, proliferation, angiogenesis, and survival pathways
Chang et al., Cancer Lett 2013 (Neoplasms) : This inhibitory effect was mediated by both autophagy ( via inhibition of mTOR and activation of p70S6K ) and apoptosis ( via caspase-3 activation ), both of which contributed to cell death and suppression of tumorigenicity