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Studies indicate that understanding mTOR network circuitry will provide insight into its deregulation in diabetes, cancer, and cardiovascular disease, but modeling in silico to elucidate how insulin activates mTORC2 remains poorly defined.
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Data reveal that LAT2 functions as an oncogenic protein and could regulate glutamine-dependent mTOR activation to promote glycolysis and decrease GEM sensitivity in pancreatic cancer.
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patients with a high p-mTOR (HR 1.27, p = 0.21). CONCLUSIONS: Phosphorylated mTOR is differentially expressed in localized RCC and metastasis. Elevated phosphorylation of mTOR is associated with aggressive pathologic features and unfavorable outcome
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This review is an emerging evidence that mTOR-dependent brain vascular dysfunction, a universal feature of aging, may be one of the mechanisms linking the regulation of the rate of aging to the pathogenesis of Alzheimer's disease. [review]
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Our data demonstrate that mTOR signaling is significantly dysregulated in human temporal lobe epilepsy
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Gal8 inhibits mTOR activity through its Ragulator-Rag signaling machinery.
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Findings show that high expression of the angiogenic marker, VEGF, in visceral adipocytes directly promotes vasculature in the uterus and mTOR activity in the endometrial glands, and provide evidence that VEGF-mTOR signaling drives endometrial cell growth leading to hyperplasia and cancer.
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Data suggest that ORP5/OSBPL5 promotes cell proliferation, cell motility, and invasiveness of neoplasm cells; this effect of ORP5/OSBPL5 depends on functional OSBP-related domain (ORD). ORP5/OSBPL5 is needed for activation of mTORC1 signaling and for transport of mTOR to lysosomes. (OSBPL5 = oxysterol-binding protein-related protein-5)
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evidence of how HMGB proteins contribute to ribosome-biogenesis control, with special emphasis on a common nexus to the target of rapamycin (TOR) pathway, a signaling cascade essential for cell growth and proliferation from yeast to human.
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Silencing of TRPC5 and inhibition of autophagy reverses adriamycin drug resistance in breast carcinoma via CaMKKbeta/AMPKalpha/mTOR pathway.
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L-type amino acid transporter 1 (LAT1) inhibitor, BCH reduces the phosphorylation of mechanistic target of rapamycin kinase (mTOR) in fibroblast-like synoviocytes from patients with rheumatoid arthritis. mTOR inhibitor, temsirolimus, neutralizes the stimulation of interleukin-17 on LAT1.
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These results indicate that, under stressful conditions, maintained mTORC1 signaling in cancer cells promotes survival by suppressing endogenous DNA damage, and may control cell fate through the regulation of CHK1.
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Results demonstrated that ASCT2 and pmTOR protein levels were significantly higher in epithelial ovarian cancer (EOC) tissues and predicting a poor prognosis. The expression levels of ASCT2 and pmTOR in EOC were positively correlated indicating a synergistic effect on the growth and development of early EOC.
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DEPTOR interaction with mTOR represses its kinase activity and rewires the mTOR signaling pathway. [review]
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both SphK1 overexpression and S1P addition increased mTOR phosphorylation as shown by ELISA, while S1PR2 inhibition had the inverse effect. These data suggest that CerS6 and SphK1 regulate mTOR signaling in breast cancer cell proliferation. Moreover, mTOR activity can be regulated by the balance between S1P and C16ceramide, which is generated by CerS6.
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Study demonstrate that the miR-495 exerts promotive effects on GC chemosensitivity via inactivation of the mTOR signaling pathway by suppressing ERBB2. The study provides reliable evidence supporting the use of miR-495 as a novel potential target in the chemotherapy of GC.
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a functional convergence between the mTOR pathway and IFITM3 proteins at endolysosomal membranes.
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data on TFEB nucleo-cytoplasmic shuttling suggest an unpredicted role of mTOR in nuclear export.
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In this review, we assess the use of mTOR inhibitors to treat age-related pathologies, discuss possible molecular mechanisms of action where evidence is available, and consider strategies to minimize undesirable side effects.
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The expression of CXCR4 and mTOR were found to be negatively correlated with remission. Kaplan-Meier analysis indicated a significant decrease in the rate of progression-free survival (PFS) and in that of overall survival (OS) in patients positive for CXCR4 and mTOR expression.