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Data show that DNA damage-inducible transcript 4 (DDIT4) was upregulated in gastric cancer (GC) cells and tissue, and that the mitogen-activated protein kinase and p53 signaling pathways were involved in the suppression of proliferation.
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Silencing lncDDIT4 in naive CD4(+) T cells enhanced Th17 differentiation through increased activation of the DDIT4/mTOR pathway.
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DDIT4 might serve as a novel prognostic biomarker in several malignancies.
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Cellular metabolism constrains innate immune responses in preterm infants due to perturbations in the expression of PPARgamma, MALT1, DDIT4, and most of the cytokines.
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these findings uncover a novel mechanism by which PML loss may contribute to mTOR activation and cancer progression via dysregulation of basal DDIT4 gene expression.
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A microarray analysis revealed that in A3G-transduced Vero cells, several cellular transcripts were differentially expressed, suggesting that A3G regulates the expression of host factors. One of the most upregulated host cell factors, REDD1 (regulated in development and DNA damage response-1, also called DDIT4), reduced MV replication approximately 10-fold upon overexpression in Vero cells.
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This is concurrent with an increase in the expression level of DDIT4, which is an inhibitor of the mammalian target of rapamycin (mTOR) signaling pathway. these results provided a novel insight on miR1243p involvement in the biological alterations of male patients with major depressive disorder and suggested that this miRNA may also serve as a malespeci fi c target for antidepressant treatment
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DDIT4 activity is directly linked to regulation of mTOR signalling
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The HIF-1alpha-REDD1-mTOR pathway was involved in the response to hypoxia in BeWo cells. Hypoxia-induced REDD1 upregulation is mediated by a HIF-1alpha-dependent pathway. Disruption of REDD1 blocked the effects of hypoxia on suppressing mTOR and resulted in additional accumulation of HIF-1alpha in BeWo cells.
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REDD1 is overexpressed during Familial Mediterranean fever inflammatory attacks induced by physical or psychological stress
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Expression of key autophagy markers (microtubule-associated protein 1A/1B light chain 3 and autophagy protein 5) was markedly reduced in cultured human chondrocytes with REDD1 depletion.
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The production of superoxide anion in nockout-Rtp801 mouse lung fibroblasts (MLF) was lower than that in Rtp801 Wt cells after cigarette smoke extract treatment, and it was inhibited in Wt MLF by silencing nicotinamide adenine dinucleotide phosphate oxidase-4 (Nox4) expression with small interfering Nox4 RNA.
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Changes in REDD1 mRNA and protein have been observed in skeletal muscle under various physiological conditions (e.g., nutrient consumption and resistance exercise) and pathological conditions (e.g., sepsis, alcoholism, diabetes, obesity) suggesting a role for REDD1 in regulating mTORC1-dependent skeletal muscle protein metabolism. [Review]
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a novel STAT3-dependent mechanism of both IL-6-induced activation of mTOR and IL-6-dependent reversion of stress-induced inhibition of mTOR activity, is reported.
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findings implicate REDD1 as a crucial regulator of mTORC1 activity in iron-depleted cells
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C/EBPbeta promotes autophagy in PC3 cells by augmenting REDD1 expression.
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These data highlight the central role of REDD1 in regulating both protein synthesis and autophagy in skeletal muscle during sepsis.
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Findings from this study propose a REDD1-regulated mechanism in T2D skeletal muscle that may contribute to whole body insulin resistance and may be a target to improve insulin action in insulin-resistant individuals.
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REDD1 knockout (KO) mice, all skin compartments, epidermal stem, and progenitor cells were protected from atrophic effects of glucocorticoids.
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MiR-630 reduced apoptosis by downregulating several apoptotic modulators, PARP3, DDIT4, and EP300.
