Gene interactions and pathways from curated databases and text-mining

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MTOR — RPS6KB1

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Kume et al., Genes Cells 2010 : Leucine enhances mTOR mediated phosphorylation of S6K1 and 4E-BP, thereby promoting protein synthesis ... Over-expression of UBR1 or UBR2 resulted in a reduction in mTOR dependent S6K1 phosphorylation, whereas knockdown of UBR1 or UBR2 increased S6K1 phosphorylation in amino acid starved human 293T cells
Patel et al., J Biol Chem 2002 : Rapamycin inhibited the mammalian target of rapamycin (mTOR) and the subsequent activation of p70/p85 S6 protein kinase-1 (S6K1) by insulin, whereas amino acid depletion prevented insulin induction of these signaling molecules
Rosner et al., Amino Acids 2012 : Recently, we have shown that mTOR mediated phosphorylation of p70 S6K1 at T389 also regulates its nucleocytoplasmic localization
Bachmann et al., J Biol Chem 2006 : However, previously we have found that mTOR shuttles between the nucleus and cytoplasm, and we have proposed that the nucleocytoplasmic shuttling of mTOR is required for the maximal activation of S6K1
Rosner et al., Oncogene 2011 : Nucleocytoplasmic localization of p70 S6K1 , but not of its isoforms p85 and p31, is regulated by TSC2/mTOR ... The mTOR dependent phosphorylation of p70 S6K1 at T389 is essential for its nuclear localization and exclusively hyperphosphorylated p70 S6K1 can be found in the nucleus
Iijima et al., J Biol Chem 2002 : Inhibition of mTOR with rapamycin blocked the Thr-389 but not the Thr-421/Ser-424 phosphorylation of S6K1
Blancquaert et al., Mol Endocrinol 2010 : mTORC1 dependent S6K1 phosphorylation in response to both insulin and cAMP required amino acids, whereas inhibition of AMP activated protein kinase and glycogen synthase kinase 3 enhanced insulin but not cAMP effects
Hwang et al., BMB Rep 2011 (Ischemia) : The loss of TSC2, which is upstream of mTOR, activates S6K1 , promotes cell growth and survival, activates mTOR kinase activities, inhibits mTORC1 and mTORC2 via mTOR inhibitors, and suppresses S6K1 and Akt ... The loss of TSC2, which is upstream of mTOR, activates S6K1, promotes cell growth and survival, activates mTOR kinase activities, inhibits mTORC1 and mTORC2 via mTOR inhibitors, and suppresses S6K1 and Akt
Balasubramanian et al., J Biol Chem 2003 (Cardiomegaly) : Studies using specific inhibitors and dominant negative c-Raf expression in cardiomyocytes indicate that the S6K1 activation involves mTOR , MEK/ERK, and phosphatidylinositol 3-kinase pathways and is independent of protein kinase C and c-Raf
Keshwani et al., J Biol Chem 2011 : The data provide evidence for regulation of S6K1, where hydrophobic motif phosphorylation is not required for PDK1 to phosphorylate S6K1 at the activation loop, but instead activation loop phosphorylation of S6K1 is required for mTOR to phosphorylate the hydrophobic motif of S6K1
Xu et al., Dev Dyn 2009 : Down regulating mTOR and raptor reduced S6K1 phosphorylation at Thr389 in one-cell embryos ... It is proposed that mTORC1 may be involved in the control of MPF by regulating S6K1 during the early development of mouse embryos
Vary et al., Alcohol Clin Exp Res 2008 : Furthermore, the data suggest that protein synthesis in rats fed a diet containing ethanol is limited by mTOR dependent reduction in phosphorylation of S6K1 ( Thr ( 389 ) ) and eIF4G ( Ser ( 1108 ) ) secondary to reduced phosphorylation of mTOR ( Ser ( 2448 ) )
Hannan et al., Mol Cell Biol 2003 : mTOR dependent regulation of ribosomal gene transcription requires S6K1 and is mediated by phosphorylation of the carboxy-terminal activation domain of the nucleolar transcription factor UBF
Magnuson et al., Biochem J 2012 : mTORC1 ( mammalian TORC1 ) phosphorylates and activates S6K1 and S6K2, whose first identified substrate was rpS6 ( ribosomal protein S6 ), a component of the 40S ribosome
Pastor et al., J Biol Chem 2009 (Ischemia) : OGD induced apoptosis was increased by the combined deletion of S6K1 and S6K2 genes, as well as by treatment with rapamycin that inhibits S6K1 activity by acting on the upstream regulator mTOR ( mammalian target of rapamycin )
Liu et al., Oncogene 2008 : Both S6K1 and 4E-BP1 pathways, mediated by the mTOR-raptor complex , are involved in the regulation of IGF-I stimulated F-actin reorganization, but only the former controls IGF-I stimulated phosphorylation of the focal adhesion proteins
Tang et al., Biochem J 2003 (Astrocytoma...) : This response was blocked by rapamycin, but was not markedly affected by 100 nM wortmannin, implying separate roles for mTOR and PI3K in S6K1 activation
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
Matsushima et al., J Biol Chem 2006 : In cultured cells, overexpression of TRB3 completely inhibited insulin stimulated S6K1 activation by mammalian target of rapamycin , whereas knockdown of endogenous TRB3 increased both basal and insulin stimulated activity
Ohguchi et al., J Cell Physiol 2005 (Melanoma) : The activity of mammalian target of rapamycin (mTOR) is essential for phosphorylation of S6K1 and the treatment malanoma cells with rapamycin, a potent inhibitor of mTOR effectively induced melanogenesis
Dibble et al., Mol Cell Biol 2009 : We find that Rictor-T1135 is directly phosphorylated by the mTORC1 dependent kinase S6K1
Prizant et al., J Cell Biochem 2008 : This confirms specific mTORC1 regulation of S6K1 phosphorylation
Kimball et al., Am J Physiol Endocrinol Metab 2000 : The results reveal that treating 18-h fasted pigs with rapamycin, a specific inhibitor of mTOR , before feeding prevented the activation of S6K1 and the changes in eIF4F complex formation observed in skeletal muscle and liver after feeding
Dunlop et al., Autophagy 2011 : Despite this evidence for heightened mTORC1 kinase activity following ULK1 overexpresssion, mTORC1 mediated phosphorylation of S6K1 and 4E-BP1 is significantly inhibited
Chen et al., American journal of physiology. Renal physiology 2009 (Diabetes Mellitus, Experimental...) : Thus the present study provides the first genetic evidence that S6K1 plays a major role in the development of compensatory renal hypertrophy as well as diabetic renal hypertrophy and indicates that UNX- and diabetes mediated mTOR activation can selectively activate S6K1 without activating S6K2
Sarbassov et al., Curr Biol 2004 : Consistent with this finding, the rictor containing mTOR complex contains GbetaL but not raptor and it neither regulates the mTOR effector S6K1 nor is it bound by FKBP12-rapamycin
Byfield et al., J Biol Chem 2005 : S6K1 is activated by growth factors such as insulin, and by mammalian target of rapamycin (mTOR) , which is itself regulated by amino acids
Jin et al., Cell death & disease 2012 (Carcinoma, Non-Small-Cell Lung...) : AMPK induced mTOR inhibition, in turn, resulted in downregulation of ribosome protein S6 kinase 1 (S6K1) activity
Yip et al., Mol Cell 2010 : Extended incubation with FKBP12-rapamycin compromises the structural integrity of mTORC1 in a stepwise manner, leading us to propose a model in which rapamycin inhibits mTORC1 mediated phosphorylation of 4E-BP1 and S6K1 through different mechanisms
Jaeschke et al., J Cell Biol 2002 (Tuberous Sclerosis) : Although activation of wild-type S6K1 and cell proliferation in TSC2-deficient cells is dependent on the mammalian target of rapamycin (mTOR) , by using an S6K1 variant ( GST-DeltaC-S6K1 ), which is uncoupled from mTOR signaling, we demonstrate that TSC1-2 does not inhibit S6K1 via mTOR
Schalm et al., Curr Biol 2002 : The molecular basis of mTOR regulation of S6K1 and 4E-BP1 remains controversial ... The TOS motif is essential for S6K1 activation by mTOR , as mutations in this motif mimic the effect of rapamycin on S6K1 phosphorylation, and render S6K1 insensitive to changes in amino acids
Pardo et al., Oncogene 2001 (Carcinoma, Small Cell...) : Inhibition of the mammalian target of rapamycin with 10 ng/ml rapamycin blocked S6K1 activation and proliferation of both lines
Schalm et al., J Biol Chem 2005 : We have identified a conserved C-terminal `` RSPRR '' sequence that is responsible for an mTOR dependent suppression of S6K1 activation
Fingar et al., Mol Cell Biol 2004 : Here we demonstrate that restoration of mTOR signaling ( by using a rapamycin-resistant mutant of mTOR ) rescues rapamycin inhibited G ( 1 ) -phase progression, and restoration of signaling along the mTOR dependent S6K1 or 4E-BP1/eukaryotic translation initiation factor 4E ( eIF4E ) pathways provides partial rescue
Holz et al., J Biol Chem 2005 : Expression of a constitutively active, rapamycin- and wortmannin-resistant S6K1 leads to constitutive phosphorylation of mTOR , whereas knock-down of S6K1 using small inhibitory RNA greatly reduces mTOR phosphorylation despite elevated Akt activity
Zito et al., J Biol Chem 2007 : S 6 ribosomal kinase 1 (S6K1) , which is activated by the mammalian target of rapamycin , is critical for cell growth
Akcakanat et al., Biochem Biophys Res Commun 2007 : mTORC1 is rapamycin-sensitive, and results in phosphorylation of 4E-BP1 and S6K1
Vary et al., Mol Cell Biochem 2005 : Activation of the potential upstream regulators of 4E-BP1 and S6K1 phosphorylation via PKB and mTOR was also observed
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
Ohguchi et al., Biochem Biophys Res Commun 2006 : The activity of mammalian target of rapamycin (mTOR) is essential for phosphorylation of S6K1 and the treatment of dermal fibroblasts with rapamycin, a potent inhibitor of mTOR abolished procollagen I production