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Journal articles on the topic 'MTOR'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

López, Esther, Alejandro Berna-Erro, Javier J. López, et al. "Role of mTOR1 and mTOR2 complexes in MEG-01 cell physiology." Thrombosis and Haemostasis 114, no. 11 (2015): 969–81. http://dx.doi.org/10.1160/th14-09-0727.

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SummaryThe function of the mammalian target of rapamycin (mTOR) is upregulated in response to cell stimulation with growing and differentiating factors. Active mTOR controls cell proliferation, differentiation and death. Since mTOR associates with different proteins to form two functional macromolecular complexes, we aimed to investigate the role of the mTORI and mTOR2 complexes in MEG-01 cell physiology in response to thrombopoietin (TPO). By using mTOR antagonists and overexpressing FKBP38, we have explored the role of both mTOR complexes in proliferation, apoptosis, maturation-like mechanis

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2

Białoń, Natalia, Krzysztof Suszyński, Mikołaj Górka, et al. "Szlak mTOR i zwierzęta transgeniczne z delecją genu TSC w procesie regeneracji układu nerwowego i wybranych modelach uszkodzeń nerwu kulszowego." Postępy Biochemii 69, no. 3 (2023): 159–69. http://dx.doi.org/10.18388/pb.2021_489.

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Urazowe uszkodzenia układu nerwowego od lat są powszechnym zjawiskiem, które obniżają jakość życia pacjentów. Szlak mTOR (ang. mammalian target of rapamycin) pełni kluczową rolę w fizjologii układu nerwowego, między innymi poprzez kontrolę przeżywania i różnicowania komórek nerwowych. Nadmierna aktywacja szlaku mTOR prowadzi do wzrostu aktywności białek cyklu komórkowego i apoptozy komórek nerwowych. Ponadto, aktualne odkrycia sugerują udział szlaku mTOR w neuroplastyczności. Wykorzystanie zwierząt transgenicznych z delecją genu TSC jak i różnych modeli uszkodzeń nerwu kulszowego, pozwala na a

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3

Wang, Xueyu, Zhiqiang Wei, Yongfang Jiang, Zhongji Meng, and Mengji Lu. "mTOR Signaling: The Interface Linking Cellular Metabolism and Hepatitis B Virus Replication." Virologica Sinica 36, no. 6 (2021): 1303–14. http://dx.doi.org/10.1007/s12250-021-00450-3.

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AbstractMammalian target of rapamycin (mTOR) is a conserved Ser/Thr kinase that includes mTOR complex (mTORC) 1 and mTORC2. The mTOR pathway is activated in viral hepatitis, including hepatitis B virus (HBV) infection-induced hepatitis. Currently, chronic HBV infection remains one of the most serious public health issues worldwide. The unavailability of effective therapeutic strategies for HBV suggests that clarification of the pathogenesis of HBV infection is urgently required. Increasing evidence has shown that HBV infection can activate the mTOR pathway, indicating that HBV utilizes or hija

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4

Felkai, Luca, Ildikó Krencz, Dorottya Judit Kiss, et al. "Characterization of mTOR Activity and Metabolic Profile in Pediatric Rhabdomyosarcoma." Cancers 12, no. 7 (2020): 1947. http://dx.doi.org/10.3390/cancers12071947.

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mTOR activation has been observed in rhabdomyosarcoma (RMS); however, mTOR complex (mTORC) 1 inhibition has had limited success thus far. mTOR activation alters the metabolic pathways, which is linked to survival and metastasis. These pathways have not been thoroughly analyzed in RMSs. We performed immunohistochemistry on 65 samples to analyze the expression of mTOR complexes (pmTOR, pS6, Rictor), and several metabolic enzymes (phosphofructokinase, lactate dehydrogenase-A, β-F1-ATPase, glucose-6-phosphate dehydrogenase, glutaminase). RICTOR amplification, as a potential mechanism of Rictor ove

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5

Saran, Uttara, Michelangelo Foti, and Jean-François Dufour. "Cellular and molecular effects of the mTOR inhibitor everolimus." Clinical Science 129, no. 10 (2015): 895–914. http://dx.doi.org/10.1042/cs20150149.

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mTOR (mechanistic target of rapamycin) functions as the central regulator for cell proliferation, growth and survival. Up-regulation of proteins regulating mTOR, as well as its downstream targets, has been reported in various cancers. This has promoted the development of anti-cancer therapies targeting mTOR, namely fungal macrolide rapamycin, a naturally occurring mTOR inhibitor, and its analogues (rapalogues). One such rapalogue, everolimus, has been approved in the clinical treatment of renal and breast cancers. Although results have demonstrated that these mTOR inhibitors are effective in a

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6

Huo, Yilin, Valentina Iadevaia, and Christopher G. Proud. "Differing effects of rapamycin and mTOR kinase inhibitors on protein synthesis." Biochemical Society Transactions 39, no. 2 (2011): 446–50. http://dx.doi.org/10.1042/bst0390446.

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mTOR (mammalian target of rapamycin) forms two distinct types of complex, mTORC (mTOR complex) 1 and 2. Rapamycin inhibits some of the functions of mTORC1, whereas newly developed mTOR kinase inhibitors interfere with the actions of both types of complex. We have explored the effects of rapamycin and mTOR kinase inhibitors on general protein synthesis and, using a new stable isotope-labelling method, the synthesis of specific proteins. In HeLa cells, rapamycin only had a modest effect on total protein synthesis, whereas mTOR kinase inhibitors decreased protein synthesis by approx. 30%. This do

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7

Todeschini, Letizia, Luca Cristin, Alessandro Martinino, Amelia Mattia, Salvatore Agnes, and Francesco Giovinazzo. "The Role of mTOR Inhibitors after Liver Transplantation for Hepatocellular Carcinoma." Current Oncology 30, no. 6 (2023): 5574–92. http://dx.doi.org/10.3390/curroncol30060421.

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Liver transplantation is a treatment option for nonresectable patients with early-stage HCC, with more significant advantages when Milan criteria are fulfilled. An immunosuppressive regimen is required to reduce the risk of graft rejection after transplantation, and CNIs represent the drugs of choice in this setting. However, their inhibitory effect on T-cell activity accounts for a higher risk of tumour regrowth. mTOR inhibitors (mTORi) have been introduced as an alternative immunosuppressive approach to conventional CNI-based regimens to address both immunosuppression and cancer control. The

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8

Rivas, Donato A., Ben B. Yaspelkis, John A. Hawley та Sarah J. Lessard. "Lipid-induced mTOR activation in rat skeletal muscle reversed by exercise and 5′-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside". Journal of Endocrinology 202, № 3 (2009): 441–51. http://dx.doi.org/10.1677/joe-09-0202.

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The serine/threonine protein kinase, mammalian target of rapamycin (mTOR) is regulated by insulin and nutrient availability and has been proposed to play a central role as a nutrient sensor in skeletal muscle. mTOR associates with its binding partners, raptor and rictor, to form two structurally and functionally distinct complexes, mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2) respectively. We have investigated the assembly of mTORC1/2 and the activation of their downstream substrates (i.e. Akt, S6K1) in response to known effectors of mTOR, excess lipid availability and AMP-activated pro

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Rosborough, Brian, Dàlia Raïch-Regué, Benjamin Matta та ін. "Rapamycin-resistant mTORC1 restrains dendritic cell B7-H1 expression that requires IL-1β to enhance regulatory T cell induction (P1349)". Journal of Immunology 190, № 1_Supplement (2013): 63.27. http://dx.doi.org/10.4049/jimmunol.190.supp.63.27.

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Abstract Introduction: The mammalian Target of Rapamycin (mTOR) is a central regulator of dendritic cell (DC) function that performs the catalytic activity of mTOR complex (mTORC)1 and 2. mTORC2 functions independently from mTORC1 and is resistant to inhibition by rapamycin (RAPA); however, mTORC1 has both RAPA-sensitive and -resistant outputs. Our goal was to ascertain the role of RAPA-resistant mTOR in DC. Methods: WT C57BL/6 or B7-H1-/- bone marrow-derived DC were generated with the addition of RAPA or ATP-competitive mTOR inhibitor, which blocks all mTOR signaling. DC lacking rictor, an mT

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10

Chen, Yu-Li, Han-Wei Lin, Nai-Yun Sun, et al. "mTOR Inhibitors Can Enhance the Anti-Tumor Effects of DNA Vaccines through Modulating Dendritic Cell Function in the Tumor Microenvironment." Cancers 11, no. 5 (2019): 617. http://dx.doi.org/10.3390/cancers11050617.

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The life span of dendritic cells (DCs) can become short following induced activation, which is associated with metabolic transition due to the regulation of mechanistic target of rapamycin (mTOR). The purpose of this study was to investigate the potential of inhibiting mTOR to modulate DC functions for elevating the anti-tumor effects of DNA vaccines. Therefore, the influences of various inhibitors of mTOR (mTORi) on the expressions of DC maturation markers, the abilities of antigen presenting and processing of BMM-derived DCs and the tumor killing effects of E7-specific CD8+ T lymphocytes act

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11

Lin, Qingxiang (Nick). "Abstract B084: Overcoming drug resistance of ‘tri-complex’ pan-RAS inhibitors: Inhibition of mTOR signaling." Cancer Research 84, no. 2_Supplement (2024): B084. http://dx.doi.org/10.1158/1538-7445.panca2023-b084.

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Abstract Background: RAS mutations occur in ~20% of all cancers that drive tumor progression, and therapy targeting most predominant RAS mutations remains unavailable. Mutant-selective RAS inhibitors (RASi), such as FDA-approved KRAS G12C inhibitors, have demonstrated initial clinical responses but drug resistance frequently emerges that minimize the drug efficacy, mechanistically mediated by RAS signaling reactivation. Methods and Results: To address this challenge, we characterized a class of novel pan-RASi that universally inhibit all RAS mutations, which forms a ‘tri-complex’ with the chap

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King, Renee, Jessica Hill, Bibek Saha та ін. "Offspring of Mice Exposed to a Low-Protein Diet in Utero Demonstrate Changes in mTOR Signaling in Pancreatic Islets of Langerhans, Associated with Altered Glucagon and Insulin Expression and a Lower β-Cell Mass". Nutrients 11, № 3 (2019): 605. http://dx.doi.org/10.3390/nu11030605.

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Low birth weight is a risk factor for gestational and type 2 diabetes (T2D). Since mammalian target of rapamycin (mTOR) controls pancreatic β-cell mass and hormone release, we hypothesized that nutritional insult in utero might permanently alter mTOR signaling. Mice were fed a low-protein (LP, 8%) or control (C, 20%) diet throughout pregnancy, and offspring examined until 130 days age. Mice receiving LP were born 12% smaller and β-cell mass was significantly reduced throughout life. Islet mTOR levels were lower in LP-exposed mice and localized predominantly to α-rather than β-cells. Incubation

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13

Avniel-Polak, Shani, Gil Leibowitz, Victoria Doviner, David J. Gross, and Simona Grozinsky-Glasberg. "Combining chloroquine with RAD001 inhibits tumor growth in a NEN mouse model." Endocrine-Related Cancer 25, no. 6 (2018): 677–86. http://dx.doi.org/10.1530/erc-18-0121.

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Patients with neuroendocrine neoplasms (NENs) often require systemic treatment, which is frequently limited by the emergence of drug resistance. mTOR inhibitors (mTORi), such as RAD001 (everolimus), have been shown to inhibit neoplasm progression. mTORi stimulates autophagy, a degradation pathway that might promote the survival of neoplasm cells that are exposed to anti-cancer therapy. Chloroquine (CQ), a well-known anti-malarial and anti-rheumatic drug, suppresses autophagy. Based on our previous results, we hypothesized that CQ may enhance the anti-tumorigenic effects of mTORi by inhibiting

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Koshizuka, Keiichi, Xingyu Wu, Kuniaki Sato, et al. "Abstract 5996: Genome-wide CRISPR screening reveals a central role for ferroptotic cell death in the anti-tumor response to mTOR inhibitors in HNSCC." Cancer Research 84, no. 6_Supplement (2024): 5996. http://dx.doi.org/10.1158/1538-7445.am2024-5996.

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Abstract Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer globally, resulting in more than 300,000 deaths each year worldwide. Treatment options for HNSCC patients include surgery, radiation, chemotherapy and molecularly targeted therapies, and although immunotherapies have recently revolutionized the treatment landscape, &lt;20% of HNSCC patients respond to immune check point blockade (ICB) therapies. The survival rate of HNSCC patients has changed only modestly over the past decades, and therefore HNSCC is a significant global health problem with high mortali

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15

Marin, Philippe, Julie Meffre, and Joël Bockaert. "mTOR." médecine/sciences 29, no. 1 (2013): 28–30. http://dx.doi.org/10.1051/medsci/2013291009.

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16

Ruan, Chun, Xinxing Ouyang, Hongzhi Liu, et al. "Sin1-mediated mTOR signaling in cell growth, metabolism and immune response." National Science Review 6, no. 6 (2019): 1149–62. http://dx.doi.org/10.1093/nsr/nwz171.

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Abstract The mammalian target of rapamycin (mTOR) is an evolutionarily conserved Ser/Thr protein kinase with essential cellular function via processing various extracellular and intracellular inputs. Two distinct multi-protein mTOR complexes (mTORC), mTORC1 and mTORC2, have been identified and well characterized in eukaryotic cells from yeast to human. Sin1, which stands for Sty1/Spc1-interacting protein1, also known as mitogen-activated protein kinase (MAPK) associated protein (MAPKAP)1, is an evolutionarily conserved adaptor protein. Mammalian Sin1 interacts with many cellular proteins, but

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Ito, Daisuke, and Atsushi Kumanogoh. "mTOR Complex Signaling through the SEMA4A–Plexin B2 Axis Is Required for Optimal Activation and Differentiation of CD8+ T Cells." Journal of Immunology 196, no. 1_Supplement (2016): 199.4. http://dx.doi.org/10.4049/jimmunol.196.supp.199.4.

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Abstract Mammalian target of rapamycin (mTOR) plays crucial roles in activation and differentiation of diverse types of immune cells. Although several lines of evidence have demonstrated the importance of mTOR-mediated signals in CD4+ T cell responses, the involvement of mTOR in CD8+ T cell responses is not fully understood. In this study, we show that a class IV semaphorin, SEMA4A, regulates CD8+ T cell activation and differentiation through activation of mTOR complex (mTORC) 1. SEMA4A−/− CD8+ T cells exhibited impairments in production of IFN-γ and TNF-α and induction of the effector molecul

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18

Kilic, Banu, Meryem Temiz-Resitoglu, and Seyhan Sahan Firat. "Targeting mTOR: up-to-date mTOR inhibitors." Biorganic and Medicinal Chemistry Reports 2, no. 1-2 (2019): 1–14. http://dx.doi.org/10.25135/bmcr.16.19.09.1417.

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19

Parkman, Gennie L., Tursun Turapov, David Kircher, et al. "Abstract 427: Newer generation mTOR inhibition represents effective therapeutic strategy for BRAF-mutant melanoma." Cancer Research 83, no. 7_Supplement (2023): 427. http://dx.doi.org/10.1158/1538-7445.am2023-427.

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Abstract Despite the advent of novel therapies, the five year survival rate for Stage IV melanoma remains at only 30%. This highlights the critical need for new therapeutics to treat this refractory disease. Aberrant activation of the PI3K-AKT pathway is common in melanoma, but efforts to drug this pathway have proven largely ineffective in clinical trials. In our study, we observed that pharmacological inhibition of AKT was ineffective whereas genetic silencing of all three AKT paralogs significantly abrogated melanoma cell growth and led to apoptosis through effects on mTORC signaling. This

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Suryawan, Agus, Asumthia S. Jeyapalan, Renan A. Orellana, Fiona A. Wilson, Hanh V. Nguyen, and Teresa A. Davis. "Leucine stimulates protein synthesis in skeletal muscle of neonatal pigs by enhancing mTORC1 activation." American Journal of Physiology-Endocrinology and Metabolism 295, no. 4 (2008): E868—E875. http://dx.doi.org/10.1152/ajpendo.90314.2008.

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Skeletal muscle in the neonate grows at a rapid rate due in part to an enhanced sensitivity to the postprandial rise in amino acids, particularly leucine. To elucidate the molecular mechanism by which leucine stimulates protein synthesis in neonatal muscle, overnight-fasted 7-day-old piglets were treated with rapamycin [an inhibitor of mammalian target of rapamycin (mTOR) complex (mTORC)1] for 1 h and then infused with leucine for 1 h. Fractional rates of protein synthesis and activation of signaling components that lead to mRNA translation were determined in skeletal muscle. Rapamycin complet

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Damerill, Ian, Kyle K. Biggar, Majida Abu Shehab, Shawn Shun-Cheng Li, Thomas Jansson, and Madhulika B. Gupta. "Hypoxia Increases IGFBP-1 Phosphorylation Mediated by mTOR Inhibition." Molecular Endocrinology 30, no. 2 (2016): 201–16. http://dx.doi.org/10.1210/me.2015-1194.

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Abstract In fetal growth restriction (FGR), fetal growth is limited by reduced nutrient and oxygen supply. Insulin-like growth factor I (IGF-I) is a key regulator of fetal growth and IGF binding protein -1(IGFBP-1) is the principal regulator of fetal IGF-I bioavailability. Phosphorylation enhances IGFBP-1's affinity for IGF-I. Hypoxia induces IGFBP-1 hyperphosphorylation, markedly decreasing IGF-I bioavailability. We recently reported that fetal liver IGFBP-1 hyperphosphorylation is associated with inhibition of the mechanistic target of rapamycin (mTOR) in a nonhuman primate model of FGR. Her

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Narula, Jeremy A. Bravo, and Vito W. Rebecca. "Abstract 419: Elevated Akt/mTOR signaling drives therapy resistance in ALM." Cancer Research 83, no. 7_Supplement (2023): 419. http://dx.doi.org/10.1158/1538-7445.am2023-419.

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Abstract Metastatic acral lentiginous melanoma (ALM) is the most lethal subtype of cutaneous melanoma and effective therapies for patients have not been established. Studies revealed a link between the dysregulation of CDK4/6 and ALM mortality, however CDK4/6 inhibitors (CDK4i/6i) have proved ineffective in patients with advanced ALM. The tumor suppressor Rb was recently shown to have a novel suppressive role towards mTORC2. Here, we elucidate the role of a non-canonical tumor suppressor function of Rb in negative regulation of mTOR in CDK4i/6i-resistance. We hypothesize that the loss of Rb in

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Mparmpakas, Dionisis, Elena Zachariades, Anastasia Goumenou, Yori Gidron, and Emmanouil Karteris. "Placental DEPTOR as a stress sensor during pregnancy." Clinical Science 122, no. 7 (2011): 349–59. http://dx.doi.org/10.1042/cs20110378.

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DEPTOR [DEP-domain-containing and mTOR (mammalian target of rapamycin)-interacting protein] is a modulator of mTOR signalling that binds to mTORC (mTOR complex) 1 and mTORC2. However, to date, the precise functions of DEPTOR are not fully elucidated, particularly in reproductive tissues where mTOR acts as a placental nutrient sensor. Pregnancy is associated with major physiological and psychosocial changes and adaptation to these changes is crucial for normal fetal development. In the present study, we tested the hypothesis that maternal stress can affect mTOR signalling at term, and, as a res

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Giubellino, Alessio, Petra Bullova, Svenja Nölting, et al. "Combined Inhibition of mTORC1 and mTORC2 Signaling Pathways Is a Promising Therapeutic Option in Inhibiting Pheochromocytoma Tumor Growth: In Vitro and In Vivo Studies in Female Athymic Nude Mice." Endocrinology 154, no. 2 (2013): 646–55. http://dx.doi.org/10.1210/en.2012-1854.

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Several lines of evidence, including the recent discovery of novel susceptibility genes, point out an important role for the mammalian target of rapamycin (mTOR) signaling pathway in the development of pheochromocytoma. Analyzing a set of pheochromocytomas from patients with different genetic backgrounds, we observed and confirmed a significant overexpression of key mTOR complex (mTORC) signaling mediators. Using selective ATP-competitive inhibitors targeting both mTORC1 and mTORC2, we significantly arrested the in vitro cell proliferation and blocked migration of pheochromocytoma cells as a r

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Laplante, M., and D. M. Sabatini. "mTOR Signaling." Cold Spring Harbor Perspectives in Biology 4, no. 2 (2011): a011593. http://dx.doi.org/10.1101/cshperspect.a011593.

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Gohlisch, Christopher. "mTOR-Inhibition." Dialyse aktuell 20, no. 08 (2016): 389–92. http://dx.doi.org/10.1055/s-0042-116347.

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Haas, Michael J. "mTOR caveats." Science-Business eXchange 1, no. 6 (2008): 132. http://dx.doi.org/10.1038/scibx.2008.132.

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Ernstoff, Marc S. "mTOR Pathway and mTOR Inhibitors in Cancer Therapy." British Journal of Clinical Pharmacology 71, no. 6 (2011): 970. http://dx.doi.org/10.1111/j.1365-2125.2011.03919.x.

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Myint, Khine Nyein, Sean Wallace, Shihe Hou, et al. "Abstract 7196: Evaluation of nab-sirolimus in combination with fulvestrant or PI3K pathway inhibitors to overcome resistance in breast cancer cell lines." Cancer Research 84, no. 6_Supplement (2024): 7196. http://dx.doi.org/10.1158/1538-7445.am2024-7196.

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Abstract Background: Endocrine therapy (ET) is the standard of care for hormone receptor positive (HR+) breast cancer (BC), but ET resistance develops in most patients (pts). One resistance mechanism involves cross talk between the PI3K-AKT-mTOR and estrogen receptor (ER) signaling pathways, resulting in increased ER signaling and tumor proliferation. This is mitigated by mTOR inhibition as demonstrated by improved outcomes with exemestane plus the mTOR inhibitor (mTORi) everolimus in pts with HR+ advanced BC. While PI3K inhibitors (PI3Ki [e.g. alpelisib]) are efficacious in pts with HR+, PIK3

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Acklin, Joshua, Mitra Azadniv, Scott Portwood, et al. "Optimizing Effects of mTOR Inhibition in Acute Myelogenous Leukemia." Blood 126, no. 23 (2015): 4930. http://dx.doi.org/10.1182/blood.v126.23.4930.4930.

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Abstract Introduction : Mammalian target of rapamycin (mTOR) signaling has previously been identified as a possible therapeutic target in acute myelogenous leukemia (AML), as the PI3K/AKT/mTOR pathway has been shown to be upregulated in blasts of up to 90% of AML cases through the constitutive loss of the tumor suppressor PTEN. The activation of this pathway is implicated in synthesis of prosurvival transcription and translational factors responsible for cellular resistance to apoptosis, resistance to chemotherapy, and enhanced survival in the marrow microenvironment. Unfortunately, exploitati

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Li, Na, Jie Chen, Qiang Liu, et al. "Prognostic significance and tumor-immune infiltration of mTOR in clear cell renal cell carcinoma." PeerJ 9 (August 17, 2021): e11901. http://dx.doi.org/10.7717/peerj.11901.

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Mammalian target of rapamycin (mTOR), a serine/threonine kinase involved in cell proliferation, survival, metabolism and immunity, was reportedly activated in various cancers. However, the clinical role of mTOR in renal cell carcinoma (RCC) is controversial. Here we detected the expression and prognosis of total mTOR and phosphorylated mTOR (p-mTOR) in clear cell RCC (ccRCC) patients, and explored the interactions between mTOR and immune infiltrates in ccRCC. The protein level of mTOR and p-mTOR was determined by western blotting (WB), and their expression was evaluated in 145 ccRCC and 13 non

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Qian, Jiayi, Siyuan Su, and Pengda Liu. "Experimental Approaches in Delineating mTOR Signaling." Genes 11, no. 7 (2020): 738. http://dx.doi.org/10.3390/genes11070738.

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The mTOR signaling controls essential biological functions including proliferation, growth, metabolism, autophagy, ageing, and others. Hyperactivation of mTOR signaling leads to a plethora of human disorders; thus, mTOR is an attractive drug target. The discovery of mTOR signaling started from isolation of rapamycin in 1975 and cloning of TOR genes in 1993. In the past 27 years, numerous research groups have contributed significantly to advancing our understanding of mTOR signaling and mTOR biology. Notably, a variety of experimental approaches have been employed in these studies to identify k

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Song, Xiaoxiao, Yoichiro Kusakari, Chun-Yang Xiao, et al. "mTOR attenuates the inflammatory response in cardiomyocytes and prevents cardiac dysfunction in pathological hypertrophy." American Journal of Physiology-Cell Physiology 299, no. 6 (2010): C1256—C1266. http://dx.doi.org/10.1152/ajpcell.00338.2010.

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Previous studies have suggested that inhibition of the mammalian target of rapamycin (mTOR) by rapamycin suppresses myocardial hypertrophy. However, the role of mTOR in the progression of cardiac dysfunction in pathological hypertrophy has not been fully defined. Interestingly, recent reports indicate that the inflammatory response, which plays an important role in the development of heart failure, is enhanced by rapamycin under certain conditions. Our aim in this study was to determine the influence of mTOR on pathological hypertrophy and to assess whether cardiac mTOR regulates the inflammat

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Avruch, Joseph, Xiaomeng Long, Yenshou Lin, et al. "Activation of mTORC1 in two steps: Rheb-GTP activation of catalytic function and increased binding of substrates to raptor1." Biochemical Society Transactions 37, no. 1 (2009): 223–26. http://dx.doi.org/10.1042/bst0370223.

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The signalling function of mTOR complex 1 is activated by Rheb-GTP, which controls the catalytic competence of the mTOR (mammalian target of rapamycin) kinase domain by an incompletely understood mechanism. Rheb can bind directly to the mTOR kinase domain, and association with inactive nucleotide-deficient Rheb mutants traps mTOR in a catalytically inactive state. Nevertheless, Rheb-GTP targets other than mTOR, such as FKBP38 (FK506-binding protein 38) and/or PLD1 (phospholipase D1), may also contribute to mTOR activation. Once activated, the mTOR catalytic domain phosphorylates substrates onl

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Xu, Song, Li Li, Min Li, et al. "Impact on Autophagy and Ultraviolet B Induced Responses of Treatment with the MTOR Inhibitors Rapamycin, Everolimus, Torin 1, and pp242 in Human Keratinocytes." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–21. http://dx.doi.org/10.1155/2017/5930639.

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The mechanistic target of Rapamycin (MTOR) protein is a crucial signaling regulator in mammalian cells that is extensively involved in cellular biology. The function of MTOR signaling in keratinocytes remains unclear. In this study, we detected the MTOR signaling and autophagy response in the human keratinocyte cell line HaCaT and human epidermal keratinocytes treated with MTOR inhibitors. Moreover, we detected the impact of MTOR inhibitors on keratinocytes exposed to the common carcinogenic stressors ultraviolet B (UVB) and UVA radiation. As a result, keratinocytes were sensitive to the MTOR

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Saddadi, Fereshteh, and Mohammad Hassan Fallahkohan. "Everolimus induced pulmonary thromboembolism after kidney transplantation; a case report." Journal of Nephropathology 11, no. 1 (2021): e11-e11. http://dx.doi.org/10.34172/jnp.2022.11.

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Choice of maintenance immunosuppressive therapy after renal transplantation is important for graft survival. However, complication may also occur. Venous thromboembolic event with the mTOR inhibitor (mTORi) everolimus is a rare but life-threatening complication. Here we describe a renal transplant recipient who developed pulmonary thromboembolism.

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Dockery, Lauren E., Brian M. Slomovitz, Fernanda Musa, et al. "A phase 2, open-label, single-arm, prospective, multicenter study of nab-sirolimus plus letrozole in advanced or recurrent endometrioid endometrial cancer." Journal of Clinical Oncology 42, no. 16_suppl (2024): TPS5640. http://dx.doi.org/10.1200/jco.2024.42.16_suppl.tps5640.

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TPS5640 Background: This clinical trial is designed to evaluate the antitumor activity of nab-sirolimus in combination with letrozole in patients with advanced or recurrent endometrioid endometrial carcinoma (EEC). Despite recent pivotal data demonstrating improved outcomes with immunotherapy plus chemotherapy, regardless of mismatch repair status, alternative nonchemotherapy-based treatment options for patients with advanced or recurrent EEC remain necessary. Dysregulation of mTOR signaling is implicated in the pathology of EEC, in which >80% harbor PTEN or PI3K/Akt/mTOR pathway alteration

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Sonis, Stephen T., and Alessandro Villa. "A New Hypothesis Describing the Pathogenesis of Oral Mucosal Injury Associated with the Mammalian Target of Rapamycin (mTOR) Inhibitors." Cancers 16, no. 1 (2023): 68. http://dx.doi.org/10.3390/cancers16010068.

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It has been 24 years since rapamycin (sirolimus) was approved to mitigate solid organ transplant rejection and 16 years since mTOR (mammalian/mechanistic target of rapamycin) inhibitors reached patients as a cancer therapy. While the clinical benefits of mTOR inhibitors (mTORi) are robust, so too are their toxicities. Among the most common issues is the development of ulcers of the oral mucosa (mTOR-inhibitor associated stomatitis; mIAS). These lesions are distinct from those of other anti-cancer agents, occur with regularity, and impact patient outcomes. mIAS’ pathogenesis has been the subjec

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Marafie, Sulaiman K., Fahd Al-Mulla, and Jehad Abubaker. "mTOR: Its Critical Role in Metabolic Diseases, Cancer, and the Aging Process." International Journal of Molecular Sciences 25, no. 11 (2024): 6141. http://dx.doi.org/10.3390/ijms25116141.

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The mammalian target of rapamycin (mTOR) is a pivotal regulator, integrating diverse environmental signals to control fundamental cellular functions, such as protein synthesis, cell growth, survival, and apoptosis. Embedded in a complex network of signaling pathways, mTOR dysregulation is implicated in the onset and progression of a range of human diseases, including metabolic disorders such as diabetes and cardiovascular diseases, as well as various cancers. mTOR also has a notable role in aging. Given its extensive biological impact, mTOR signaling is a prime therapeutic target for addressin

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Wang, Tianyi, Kaiqi Long, Yang Zhou, et al. "Optochemical Control of mTOR Signaling and mTOR-Dependent Autophagy." ACS Pharmacology & Translational Science 5, no. 3 (2022): 149–55. http://dx.doi.org/10.1021/acsptsci.1c00230.

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Dowling, Ryan J. O., Ivan Topisirovic, Bruno D. Fonseca, and Nahum Sonenberg. "Dissecting the role of mTOR: Lessons from mTOR inhibitors." Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics 1804, no. 3 (2010): 433–39. http://dx.doi.org/10.1016/j.bbapap.2009.12.001.

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Gomez-Pinillos, Alejandro, and Anna C. Ferrari. "mTOR Signaling Pathway and mTOR Inhibitors in Cancer Therapy." Hematology/Oncology Clinics of North America 26, no. 3 (2012): 483–505. http://dx.doi.org/10.1016/j.hoc.2012.02.014.

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Patel, Raina A., Imran Ahmad, Christine E. Sheehan, et al. "Expression of Phosphorylated mTOR (p-mTOR) Correlates with Advanced Stage in Diffuse Large B-Cell Lymphomas." Blood 110, no. 11 (2007): 1573. http://dx.doi.org/10.1182/blood.v110.11.1573.1573.

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Abstract Background: The mammalian target of rapamycin (mTOR), plays a major role in regulating cell growth. The activated form of mTOR (phosphorylated mTOR) mediates its effects through mitogen and nutrient dependant signal transduction that regulates mRNA translation. Levels of phosphorylated mTOR (p-mTOR) have been shown to correlate with cell proliferation and inhibition of the mTOR pathway has shown therapeutic promise in some tumors. Information on the role of p-mTOR in hematopoietic malignancies is limited. The aim of the current study is to evaluate the expression of p-mTOR in diffuse

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Goodman, Craig A., Man Hing Miu, John W. Frey, et al. "A Phosphatidylinositol 3-Kinase/Protein Kinase B-independent Activation of Mammalian Target of Rapamycin Signaling Is Sufficient to Induce Skeletal Muscle Hypertrophy." Molecular Biology of the Cell 21, no. 18 (2010): 3258–68. http://dx.doi.org/10.1091/mbc.e10-05-0454.

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It has been widely proposed that signaling by mammalian target of rapamycin (mTOR) is both necessary and sufficient for the induction of skeletal muscle hypertrophy. Evidence for this hypothesis is largely based on studies that used stimuli that activate mTOR via a phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB)-dependent mechanism. However, the stimulation of signaling by PI3K/PKB also can activate several mTOR-independent growth-promoting events; thus, it is not clear whether signaling by mTOR is permissive, or sufficient, for the induction of hypertrophy. Furthermore, the presum

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Wang, Xuerong, Ping Yue, Chi-Bun Chan, et al. "Inhibition of Mammalian Target of Rapamycin Induces Phosphatidylinositol 3-Kinase-Dependent and Mnk-Mediated Eukaryotic Translation Initiation Factor 4E Phosphorylation." Molecular and Cellular Biology 27, no. 21 (2007): 7405–13. http://dx.doi.org/10.1128/mcb.00760-07.

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ABSTRACT The initiation factor eukaryotic translation initiation factor 4E (eIF4E) plays a critical role in initiating translation of mRNAs, including those encoding oncogenic proteins. Therefore, eIF4E is considered a survival protein involved in cell cycle progression, cell transformation, and apoptotic resistance. Phosphorylation of eIF4E (usually at Ser209) increases its binding affinity for the cap of mRNA and may also favor its entry into initiation complexes. Mammalian target of rapamycin (mTOR) inhibitors suppress cap-dependent translation through inhibition of the phosphorylation of e

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Machado, Luis Eduardo, Arthur William Alvarenga, Fernanda Ferreira da Silva, et al. "Overexpression of mTOR and p(240–244)S6 in IDH1 Wild-Type Human Glioblastomas Is Predictive of Low Survival." Journal of Histochemistry & Cytochemistry 66, no. 6 (2018): 403–14. http://dx.doi.org/10.1369/0022155417750838.

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Summary PI3K/Akt/mTOR pathway activation is a hallmark of high-grade gliomas, which prompted clinical trials for the use of PI3K and mTOR inhibitors. However, the poor results in the original trials suggested that better patient profiling was needed for such drugs. Thus, accurate and reproducible monitoring of mTOR complexes can lead to improved therapeutic strategies. In this work, we evaluated the expression and phosphorylation of mTOR, RAPTOR, and rpS6 in 195 human astrocytomas and 30 normal brain tissue samples. The expression of mTOR increased in glioblastomas, whereas mTOR phosphorylatio

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Guglielmelli, Tommasina, Emilia Giugliano, Vanessa Brunetto, Sokol Rrodhe, and Giuseppe Saglio. "Cytoplasmic-Nuclear Shuttling of mTOR Protein in Multiple Myeloma Cell Lines and Primary Myeloma Cells: A New Mechanism Regulated by Pomalidomide." Blood 120, no. 21 (2012): 4019. http://dx.doi.org/10.1182/blood.v120.21.4019.4019.

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Abstract Abstract 4019 Introduction. mTOR is a serine-threonine protein kinase that plays a central role in regulating critical cellular processes. Consistent with its primary target being the translation machinery, mTOR is predominantly localized in the cytoplasm. However, a nuclear localization of mTOR has been found in rhabdomyosarcomas and HCT8 colon carcinoma cells. Furthermore, mTOR becomes nuclear in HEK293 cells treated with leptomycin B, a specific inhibitor of nuclear export receptor Crm1, suggesting that mTOR may be a cytoplasmic-nuclear shuttling protein. Aims of this study is to e

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Wei, Xinyi, Sabine Weber, Decheng Yin, et al. "Pharmacodynamic Effect of mTOR Inhibition-based Immunosuppressive Therapy on T- and B-cell Subsets After Renal Transplantation." Transplantation Direct 10, no. 7 (2024): e1666. http://dx.doi.org/10.1097/txd.0000000000001666.

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Background. The mammalian target of rapamycin inhibitor (mTORi) therapy after kidney transplantation is solely monitored pharmacokinetically, not necessarily reflecting PI3K-Akt-mTOR pathway blockade efficacy leading to potential under-or overimmunosuppression. Methods. In this cross-sectional study, phosphoflow cytometry was used to determine the efficacy of mTOR inhibition in peripheral T- and B-lymphocyte subsets by assessing p70S6 kinase (p70S6K) phosphorylation in renal transplant recipients upon treatment with a combination of either mTORi and calcineurin inhibitors (n = 18), or mTORi wi

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Cheng, Sze, Naima Ahmed Fahmi, Meeyeon Park, et al. "mTOR Contributes to the Proteome Diversity through Transcriptome-Wide Alternative Splicing." International Journal of Molecular Sciences 23, no. 20 (2022): 12416. http://dx.doi.org/10.3390/ijms232012416.

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The mammalian target of rapamycin (mTOR) pathway is crucial in energy metabolism and cell proliferation. Previously, we reported transcriptome-wide 3′-untranslated region (UTR) shortening by alternative polyadenylation upon mTOR activation and its impact on the proteome. Here, we further interrogated the mTOR-activated transcriptome and found that hyperactivation of mTOR promotes transcriptome-wide exon skipping/exclusion, producing short isoform transcripts from genes. This widespread exon skipping confers multifarious regulations in the mTOR-controlled functional proteomics: AS in coding reg

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Che, Xiangyu, Xiaochen Qi, Yingkun Xu, Qifei Wang, and Guangzhen Wu. "Genomic and Transcriptome Analysis to Identify the Role of the mTOR Pathway in Kidney Renal Clear Cell Carcinoma and Its Potential Therapeutic Significance." Oxidative Medicine and Cellular Longevity 2021 (June 7, 2021): 1–28. http://dx.doi.org/10.1155/2021/6613151.

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The mTOR pathway, a major signaling pathway, regulates cell growth and protein synthesis by activating itself in response to upstream signals. Overactivation of the mTOR pathway may affect the occurrence and development of cancer, but no specific treatment has been proposed for targeting the mTOR pathway. In this study, we explored the expression of mTOR pathway genes in a variety of cancers and the potential compounds that target the mTOR pathway and focused on an abnormal type of cancer, kidney renal clear cell carcinoma (KIRC). Based on the mRNA expression of the mTOR pathway gene, we divid

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