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DDIT4 — MTOR

Text-mined interactions from Literome

Brugarolas et al., Genes Dev 2004 (Anoxia) : Here we show that mTOR inhibition by hypoxia requires the TSC1/TSC2 tumor suppressor complex and the hypoxia-inducible gene REDD1/RTP801
Sofer et al., Mol Cell Biol 2005 : Regulation of mTOR and cell growth in response to energy stress by REDD1 ... REDD1 likely acts on the TSC1/2 complex, as regulation of mTOR substrate phosphorylation by REDD1 requires TSC2 and is blocked by overexpression of the TSC1/2 downstream target Rheb but is not blocked by inhibition of AMPK
DeYoung et al., Genes Dev 2008 (Breast Neoplasms) : Endogenous REDD1 is required for both dissociation of endogenous TSC2/14-3-3 and inhibition of mTORC1 in response to hypoxia
McGhee et al., J Nutr 2009 (Diabetes Mellitus, Experimental...) : Overall, the results demonstrate that changes in REDD1 expression likely contribute to the regulation of mTORC1 signaling during food deprivation and refeeding
Jin et al., Free Radic Biol Med 2009 : In our experiment, overexpression of ATF4 was associated with reduced mTOR activity via Redd1 expression, whereas suppression of ATF4 levels with small interfering RNA led to the recovery of decreased mTOR activity mediated by downregulation of Redd1 during oxidative and ER stress
Katiyar et al., EMBO Rep 2009 : REDD1 , an inhibitor of mTOR signalling, is regulated by the CUL4A-DDB1 ubiquitin ligase
Wu et al., Endocrinology 2010 (Muscular Atrophy) : Testosterone completely prevented the 22-fold increase in expression of the mammalian target of rapamycin (mTOR) inhibitor regulated in development and DNA damage responses 1 ( REDD1 ), and attenuated dexamethasone induced increased expression of eIF4E binding protein 1, Forkhead box O1, and the p85 regulatory subunit of the IGF-I receptor but prevented decreased expression of IRS-1
Vega-Rubin-de-Celis et al., Biochemistry 2010 : REDD1 is induced by hypoxia, and REDD1 overexpression is sufficient to inhibit mTORC1 ... REDD1 induced-mTORC1 inhibition requires the TSC1/TSC2 complex, and REDD1 has been proposed to act by directly binding to and sequestering 14-3-3 proteins away from TSC2 leading to TSC2 dependent inhibition of mTORC1 ... Sequence conservation mapping to the surface of the structure and mutagenesis studies demarcated a hotspot likely to interact with effector proteins that is essential for REDD1 mediated mTORC1 inhibition
Lisse et al., FASEB J 2011 (Bone Neoplasms...) : Among these was the gene for DNA-damage-inducible transcript 4 ( DDIT4 ), an inhibitor of mammalian target of rapamycin (mTOR) signaling ... DDIT4 , an inhibitor of mTOR signaling , is a direct target for 1,25 ( OH ) ( 2 ) D ( 3 ) and VDRE-BP, and functions to suppress cell proliferation in response to vitamin D
Malagelada et al., J Neurosci 2011 : Here, we show that expression of RTP801/REDD1 , an inhibitor of mTOR ( mammalian target of rapamycin ) activation, is regulated during neuronal differentiation and that RTP801 functions to influence the timing of both neurogenesis and neuron migration
Wolff et al., Mol Cell Biol 2011 (Anoxia) : Cell-type dependent regulation of mTORC1 by REDD1 and the tumor suppressors TSC1/TSC2 and LKB1 in response to hypoxia ... We previously reported that mTORC1 regulation by hypoxia involves Redd1 and the Tsc1/Tsc2 complex
Jin et al., Oncogene 2011 : TXNIP potentiates Redd1 induced mTOR suppression through stabilization of Redd1 ... Overexpression of TXNIP was associated with reduced mTOR activity mediated by an increase in Redd1 level, whereas knockdown of TXNIP using small interfering RNA resulted in recovery of mTOR activity via downregulation of Redd1 during treatment with 2-DG
Molitoris et al., J Biol Chem 2011 : In support of this hypothesis, RNAi mediated suppression of Dig2/RTP801/REDD1 reduces mTOR inhibition and autophagy in glucocorticoid treated lymphocytes
Kucejova et al., Mol Cancer Res 2011 (Carcinoma, Renal Cell) : REDD1 is upregulated by hypoxia-inducible factor (HIF)-1, and forced REDD1 expression is sufficient to inhibit mTORC1 ... REDD1 induced mTORC1 inhibition is dependent on a protein complex formed by the tuberous sclerosis complex (TSC)1 and 2 ( TSC2 ) proteins ... In clear-cell renal cell carcinoma ( ccRCC ), the von Hippel-Lindau (VHL) gene is frequently inactivated leading to constitutive activation of HIF-2 and/or HIF-1, which may be expected to upregulate REDD1 and inhibit mTORC1 ... Understanding how ccRCCs become refractory to REDD1 induced mTORC1 inhibition should shed light into the development of ccRCC and may aid in patient selection for molecular targeted therapies
Vadysirisack et al., Mol Cell Biol 2011 : We show that Redd1 loss leads to elevated mammalian TORC1 (mTORC1) activity, which explains the increased p53 translation and protein levels ... Together, these findings suggest that REDD1 mediated suppression of mTORC1 activity exerts feedback control on p53, thereby limiting the apoptotic response and contributing to cellular survival following DNA damage
Vadysirisack et al., Methods Mol Biol 2012 : Our work has demonstrated that the stress induced protein REDD1 is essential for hypoxia regulation of mTORC1 activity and has further defined the molecular mechanism whereby REDD1 represses mTORC1 activity under hypoxic stress ... Our work has demonstrated that the stress induced protein REDD1 is essential for hypoxia regulation of mTORC1 activity and has further defined the molecular mechanism whereby REDD1 represses mTORC1 activity under hypoxic stress
Zhou et al., Mol Biol Cell 2012 : We identified REDD1 , a negative regulator of mammalian target of rapamycin (mTOR) through the tuberous sclerosis complex ( TSC1/2 complex ), as a new molecular target of NFATc3 ... We show that treatment with a combination of phorbol 12-myristate 13-acetate ( PMA ) plus ionophore A23187 ( Io ), which induces NFAT activation, increased REDD1 mRNA and protein expression and inhibited mTOR signaling ; pretreatment with the calcineurin inhibitor cyclosporin A ( CsA ), an antagonist of NFAT signaling, decreased REDD1 induction and mTOR inhibition ... We show that treatment with a combination of phorbol 12-myristate 13-acetate ( PMA ) plus ionophore A23187 ( Io ), which induces NFAT activation, increased REDD1 mRNA and protein expression and inhibited mTOR signaling ; pretreatment with the calcineurin inhibitor cyclosporin A ( CsA ), an antagonist of NFAT signaling, decreased REDD1 induction and mTOR inhibition
Kelleher et al., Am J Physiol Endocrinol Metab 2013 : In conclusion, the results show an immobilization induced attenuation of mTORC1 signaling mediated by induction of REDD1/2 and defective p70S6K1 phosphorylation
Regazzetti et al., PloS one 2012 (MAP Kinase Signaling System) : In 3T3-L1 adipocytes, silencing of REDD1 with siRNA induces an increase of mTORC1 activity as well as an inhibition of insulin signaling pathway and lipogenesis
Jin et al., Cancer Lett 2013 (Lung Neoplasms) : Herein, we show that the constitutive overexpression of Redd1 , a negative regulator of mTORC1 , induces Akt activation in lung cancer cells ... Therefore, the sustained overexpression of Redd1 leads to mTORC1 inhibition and to consequent Akt activation that is involved in cell survival
Tan et al., PloS one 2013 : In this study, we discovered that mTORC1 regulates REDD1 protein stability in a 26S proteasome dependent manner ... Inhibition of mTORC1 resulted in reduced REDD1 protein stability and a consequent decrease in REDD1 expression