Relevant bibliographies by topics / MTOR

Academic literature on the topic 'MTOR'

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Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "MTOR"

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López, Esther, Alejandro Berna-Erro, Javier J. López, María P. Granados, Nuria Bermejo, José M. Brull, Ginés M. Salido, Juan A. Rosado, and Pedro C. Redondo. "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 mechanisms, endoplasmic reticulum-stress and the intracellular location of both active mTOR complexes during MEG-01 cell stimulation with TPO. The results demonstrate that mTOR1 and mTOR2 complexes play different roles in the physiology of MEG-01 cells and in the maturation-like mechanisms; hence, these findings might help to understand the mechanism underlying generation of platelets.
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Białoń, Natalia, Krzysztof Suszyński, Mikołaj Górka, Michał Trzęsicki, Dariusz Górka, Kacper Zając, and Agata Kupczak. "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 (September 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 aktywację szlaku mTOR. Obecnie wyniki badań potwierdzają, iż inaktywacja mutacji punktowych w genach TSC-1 lub TSC-2 aktywuje kanoniczną ścieżkę sygnałową kompleksu mTORC-1, z kolei reaktywacja szlaku mTORC-1 poprzez absencję genu TSC-1 w dojrzałych neuronach indukuje regenerację aksonów. Zaburzenia funkcji szlaku mTORC-1 w komórkach Schwanna hamują mielinizację włókien nerwowych. Celem niniejszej pracy jest usystematyzowanie wiedzy i przedstawienie roli szlaku mTOR, jak również wykazanie roli delecji genu TSC w procesie regeneracji układu nerwowego. Obecne badania nad aktywnością szlaku mTOR mogą zapewnić nowe strategie intensyfikowania regeneracji nerwów obwodowych.
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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 (September 28, 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 hijacks the mTOR pathway to benefit its own replication. Therefore, the mTOR signaling pathway might be a crucial target for controlling HBV infection. Here, we summarize and discuss the latest findings from model biology research regarding the interaction between the mTOR signaling pathway and HBV replication.
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Felkai, Luca, Ildikó Krencz, Dorottya Judit Kiss, Noémi Nagy, Gábor Petővári, Titanilla Dankó, Tamás Micsík, et al. "Characterization of mTOR Activity and Metabolic Profile in Pediatric Rhabdomyosarcoma." Cancers 12, no. 7 (July 17, 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 overexpression, was analyzed by FISH and digital droplet PCR. In total, 64% of the studied primary samples showed mTOR activity with an mTORC2 dominance (82%). Chemotherapy did not cause any relevant change in mTOR activity. Elevated mTOR activity was associated with a worse prognosis in relapsed cases. RICTOR amplification was not confirmed in any of the cases. Our findings suggest the importance of the Warburg effect and the pentose-phosphate pathway beside a glutamine demand in RMS cells. The expression pattern of the studied mTOR markers can explain the inefficacy of mTORC1 inhibitor therapy. Therefore, we suggest performing a detailed investigation of the mTOR profile before administering mTORC1 inhibitor therapy. Furthermore, our findings highlight that targeting the metabolic plasticity could be an alternative therapeutic approach.
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Saran, Uttara, Michelangelo Foti, and Jean-François Dufour. "Cellular and molecular effects of the mTOR inhibitor everolimus." Clinical Science 129, no. 10 (September 1, 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 attenuating cell growth of cancer cells under in vitro and in vivo conditions, subsequent sporadic response to rapalogues therapy in clinical trials has promoted researchers to look further into the complex understanding of the dynamics of mTOR regulation in the tumour environment. Limitations of these rapalogues include the sensitivity of tumour subsets to mTOR inhibition. Additionally, it is well known that rapamycin and its rapalogues mediate their effects by inhibiting mTORC (mTOR complex) 1, with limited or no effect on mTORC2 activity. The present review summarizes the pre-clinical, clinical and recent discoveries, with emphasis on the cellular and molecular effects of everolimus in cancer therapy.
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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 (March 22, 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 does not seem to be due to the ability of mTOR kinase inhibitors to block the binding of eIFs (eukaryotic initiation factors) eIF4G and eIF4E. Analysis of the effects of the inhibitors on the synthesis of specific proteins showed a spectrum of behaviours. As expected, synthesis of proteins encoded by mRNAs that contain a 5′-TOP (5′-terminal oligopyrimidine tract) was impaired by rapamycin, but more strongly by mTOR kinase inhibition. Several proteins not known to be encoded by 5′-TOP mRNAs also showed similar behaviour. Synthesis of proteins encoded by ‘non-TOP’ mRNAs was less inhibited by mTOR kinase inhibitors and especially by rapamycin. The implications of our findings are discussed.
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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 (June 9, 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 PI3K-AKT-mTOR signalling pathway regulates protein translation, cell growth, and metabolism, and the pathway is frequently deregulated in human tumours. Several studies have suggested the role of mTORi in reducing HCC progression after LT, accounting for a lower recurrence rate. Furthermore, mTOR immunosuppression controls the renal damage associated with CNI exposure. Conversion to mTOR inhibitors is associated with stabilizing and recovering renal dysfunction, suggesting an essential renoprotective effect. Limitations in this therapeutic approach are related to their negative impact on lipid and glucose metabolism as well as on proteinuria development and wound healing. This review aims to summarize the roles of mTORi in managing patients with HCC undergoing LT. Strategies to overcome common adverse effects are also proposed.
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Rivas, Donato A., Ben B. Yaspelkis, John A. Hawley, and 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, no. 3 (July 2, 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 protein kinase (AMPK) activation/exercise training in rat skeletal muscle. The in vivo formation of mTORC1 and 2 and the activation of their respective downstream substrates were increased in response to chronic (8 weeks) consumption of a high-fat diet. Diet-induced mTORC activation and skeletal muscle insulin resistance were reversed by 4 weeks of exercise training, which was associated with enhanced muscle AMPK activation. In order to determine whether AMPK activation reverses lipid-induced mTOR activation, L6 myotubes were exposed to 0.4 mM palmitate to activate mTORC1/2 in the absence or presence of 5′-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR). Palmitate exposure (4 h) increased insulin-stimulated S6K1 Thr389 phosphorylation by 60%, indicating activation of mTORC1. AMPK activation with 1 mM AICAR abolished lipid-induced mTOR activation in vitro. Our data implicates reductions in mTOR complex activation with the reversal of lipid-induced skeletal muscle insulin resistance in response to exercise training or AICAR and identifies mTOR as a potential target for the treatment of insulin resistance.
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Rosborough, Brian, Dàlia Raïch-Regué, Benjamin Matta, Keunwook Lee, Mark Boothby, Heth Turnquist, and Angus Thomson. "Rapamycin-resistant mTORC1 restrains dendritic cell B7-H1 expression that requires IL-1β to enhance regulatory T cell induction (P1349)." Journal of Immunology 190, no. 1_Supplement (May 1, 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 mTORC2-specific subunit, were generated from conditional rictor KO mice. DC induction of regulatory T cells (Treg) was determined in MLR, using BALB/c CD4+CD25- T cell responders. Results and Conclusion: RAPA and mTORC2 deletion reduced DC B7-H1 expression, but ATP-competitive mTOR inhibitors enhanced B7-H1 expression. Augmented B7-H1 expression was blocked by STAT3 inhibition and correlated with reduced expression of the STAT3 negative regulator, SOCS3. DC exposed to ATP-competitive mTOR inhibitors increased Treg induction, which was dependent on DC B7-H1. IL-1β neutralization additionally reduced Treg induction by B7-H1-/- ATP-competitive mTOR inhibitor-exposed DC, suggesting that IL-1β and B7-H1 act additively to promote Treg induction by these DC. These findings establish a RAPA-resistant mTORC1 pathway that acts through SOCS3 and STAT3 to regulate DC B7-H1 expression and Treg induction.
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Chen, Yu-Li, Han-Wei Lin, Nai-Yun Sun, Jr-Chi Yie, Hsueh-Chih Hung, Chi-An Chen, Wei-Zen Sun, and Wen-Fang Cheng. "mTOR Inhibitors Can Enhance the Anti-Tumor Effects of DNA Vaccines through Modulating Dendritic Cell Function in the Tumor Microenvironment." Cancers 11, no. 5 (May 2, 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 activated by BMM-derived DCs were in vitro examined. The anti-tumor effects of connective tissue growth factor (CTGF)/E7 DNA vaccine and/or mTORi were also in vivo analyzed. In our study, suppressive effects of mTORi on the DC maturation markers expressed on BMMCs could be reversed. The mTORi-treated mature BMM-derived DCs tended to be non-apoptotic. These mTORi-treated BMM-derived DCs could have better antigen presenting and processing abilities. The E7-specific cytotoxic CD8+ T lymphocytes could have more potent tumoricidal activity following activation of mTORi-treated BMM-derived DCs. For tumor-bearing mice, those treated with CTGF/E7 DNA vaccine and mTORi indeed can have higher percentages of mature DCs in the TME, better disease control and longer survivals. Consequently, application of mTORi can be a pharmacological approach for temporally increasing life span, antigen presenting and antigen processing of DCs to strengthen the therapeutic outcome of cancer immunotherapy.
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Dissertations / Theses on the topic "MTOR"

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Olsen, Jessica M. "β-Adrenergic Signalling Through mTOR." Doctoral thesis, Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-142169.

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Adrenergic signalling is part of the sympathetic nervous system and is activated upon stimulation by the catecholamines epinephrine and norepinephrine. This regulates heart rate, energy mobilization, digestion and helps to divert blood flow to important organs. Insulin is released to regulate metabolism of carbohydrates, fats and proteins, mainly by taking up glucose from the blood. The insulin and the catecholamine hormone systems are normally working as opposing metabolic regulators and are therefore thought to antagonize each other. One of the major regulators involved in insulin signalling is the mechanistic target of rapamycin (mTOR). There are two different complexes of mTOR; mTORC1 and mTORC2, and they are essential in the control of cell growth, metabolism and energy homeostasis. Since mTOR is one of the major signalling nodes for anabolic actions of insulin it was thought that catecholamines might oppose this action by inhibiting the complexes. However, lately there are studies demonstrating that this may not be the case. mTOR is for instance part of the adrenergic signalling pathway resulting in hypertrophy of cardiac and skeletal muscle cells and inhibition of smooth muscle relaxation and helps to regulate browning in white adipose tissue and thermogenesis in brown adipose tissue (BAT). In this thesis I show that β-adrenergic signalling leading to glucose uptake occurs independently of insulin in skeletal muscle and BAT, and does not activate either Akt or mTORC1, but that the master regulator of this pathway is mTORC2. Further, my co-workers and I demonstrates that β-adrenergic stimulation in skeletal muscle and BAT utilizes different glucose transporters. In skeletal muscle, GLUT4 is translocated to the plasma membrane upon stimulation. However, in BAT, β-adrenergic stimulation results in glucose uptake through translocation of GLUT1. Importantly, in both skeletal muscle and BAT, the role of mTORC2 in β-adrenergic stimulated glucose uptake is to regulate GLUT-translocation.

At the time of the doctoral defense, the following paper was unpublished and had a status as follows: Paper 4: Manuscript.

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Schalm, Stefanie. "Molecular mechanism of mTOR downstream signaling." [S.l. : s.n.], 2003. http://www.diss.fu-berlin.de/2003/249/index.html.

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Joyce, Claire Lois. "Tumour cell responses to mTOR inhibition." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610245.

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März, Andreas. "A new player in mTOR regulation." Diss., Ludwig-Maximilians-Universität München, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-139523.

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Lee, John Hung. "Altered mTOR signaling in Huntington's Disease." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/5547.

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Huntington's Disease (HD) is caused by a polyglutamine tract expansion in huntingtin (HTT). Despite HTTs ubiquitous expression, there is selective vulnerability in a specific brain region known as the striatum, the cause of which is poorly understood. Here, we provide evidence that impaired striatal mTORC1 activity underlies varied metabolic and degenerative phenotypes in striatal tissues from HD mouse models and patients, and show that further mTORC1 impairment in mouse models, achieved through the knockdown of Rhes, a striatum-enriched mTORC1 activator, exacerbates disease phenotypes. In contrast, exogenous addition of Rhes or the constitutively active form of the mTORC1 regulator, Rheb, into HD mouse brain, alleviates mitochondrial dysfunction, aberrant cholesterol homeostasis, striatal atrophy, and elicits increased autophagy, and reverses impaired dopamine signaling. Furthermore, while HD has been considered primarily a neurological disease, organs with high metabolic demand, such as heart, are also severely affected. The mechanism by which mHTT disrupts cardiac function remains unknown. I provide evidence that mTORC1 is impaired in HD mouse model hearts, causing hyperactive FoxO1 signaling which may render HD hearts vulnerable to stress induced cardiomyopathy. In sum, my combined work indicates impaired mTORC1 signaling as a primary mechanism underlying the neurodegenerative and heart-related disease phenotypes in HD, and thus presents a rational therapeutic target.
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Ramsbottom, Ben Alan. "Regulation of pol III transcription by mTOR." Thesis, University of Glasgow, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.438962.

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Pimentel, Gustavo Duarte 1983. "Caracterização da AMPK/mTOR hipotalâmica na anorexia induzida pelo câncer : Characterization of hypothalamic AMPK/mTOR in cancer-induced anorexia." [s.n.], 2015. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312747.

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Orientador: Jose Barreto Campello Carvalheira
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-26T11:52:05Z (GMT). No. of bitstreams: 1 Pimentel_GustavoDuarte_D.pdf: 5245849 bytes, checksum: ec5c43602ec0d60564455aae4b1fee3a (MD5) Previous issue date: 2015
Resumo: A teoria das doenças geradas por citocinas inflamatórias trouxe ao longo dos anos indícios que o organismo pode produzir citocinas que desempenham respostas biológicas benéficas ou prejudiciais. Com o passar dos anos ficou claro que a inflamação é um mecanismo chave na fisiopatologia do câncer. Interessantemente, diversos estudos sugerem que a AMPK e mTOR hipotalâmica, importantes moléculas no controle do balanço energética também seja responsável por modular a inflamação e anorexia. Nesse sentido, foi observado: 1) A inibição da AMPK hipotalâmica proporciona redução do peso corporal e da inflamação central e periférica potencializando o crescimento tumoral. Por outro lado, a ativação da AMPK com AICAR, salicilato e vetor viral reverte à anorexia induzida pelo câncer. Entretanto, os efeitos benéficos do AICAR foram bloqueados quando associados com os antagonistas colinérgicos, sugerindo que a AMPK no núcleo ventromedial é responsável pelo controle da anorexia e inflamação. 2) A AMPK no núcleo ventromedial do hipotálamo, principalmente a isoforma alfa 1 ativa a termogênese aumentando a produção de calor na qual converte tecido adiposo branco em bege. Além disso, o uso do antagonista ?3 adrenérgico ou a ativação da AMPK foram capazes de atenuar a produção de calor melhorando a caquexia induzida pelo câncer. 3) Roedores com câncer possuem a via do IKK/mTOR ativada no núcleo arqueado do hipotálamo proporcionando anorexia e caquexia. Por outro lado, o bloqueio da S6K com adenovírus foi capaz de melhorar a anorexia. Portanto, esses achados permitem concluir que o hipotálamo funciona como um centro regulador da anorexia e caquexia induzida pelo câncer, abrindo novos horizontes para o tratamento do câncer
Abstract: The theory of diseases generated by inflammatory cytokine brought over the years evidence that the organism may produce cytokine with beneficial and deleterious responses. Nowadays, it is clear that the inflammation is a key mechanism in cancer pathophysiology. Interestingly, several studies suggest that hypothalamic AMPK and mTOR, important molecules in the energy balance control also is responsible for modulation of both inflammation and anorexia. The studies presented herein observed that: 1) Inhibition of hypothalamic AMPK leads to weight loss and central and systemic inflammation which potentiates the tumor growth. However, AMPK activation with AICAR, salicylate and vector viral might reverse the cancer-mediated anorexia. Nevertheless, benefic effects of AICAR are blunted with a combination of cholinergic antagonists, suggesting that ventromedial of hypothalamus (VMH)-specific AMPK action is responsible for the anorexia and inflammation control. 2) VMH-specific AMPK, particularly the isoform alpha 1 activates thermogenesis increasing heat production which switches the white adipose tissue in beige. Furthermore, ?3 adrenergic antagonist and AMPK activation were able to attenuate the heal generation, block the "browning of WAT" and improve the cancer cachexia. 3) Cancer rats have activated IKK/mTOR pathway in arcuate nucleus (ARC) of the hypothalamus. In contrast, neutralization of S6K through adenovirus was able to improve anorexia. Therefore, our data show evidences that the hypothalamus a key center that integrates a number of mechanisms triggered by cancer-induced anorexia and -cachexia, opening new horizons for the treatment of cancer
Doutorado
Fisiopatologia Médica
Doutor em Ciências
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Wong, Jacky Sui Ki. "The Evaluation of Dual PI3K/mTOR Inhibitors as a Superior Alternative to mTOR Inhibitors in Pre-B Acute Lymphoblastic Leukaemia." Thesis, The University of Sydney, 2014. http://hdl.handle.net/2123/13644.

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Acute lymphoblastic leukaemia (ALL) is the most common form of cancer in children. Poor long term survival in adults as well as the bleak outlook for relapsed patients highlights the need for new therapeutic strategies for the treatment of ALL. The major regulators of ALL cell proliferation and survival mediate their effects through the phosphatidylinositol-3-kinase (PI3K)/mammalian target of rapamycin. It has been previously shown that the mTOR inhibitor RAD001 extended survival in a non-obese diabetic/severe combined immune deficient (NOD/SCID) mouse xenograft model of ALL. The work presented in this thesis examines the effect of the dual PI3K/mTOR inhibitors BEZ235 and BGT226 in ALL. In summary, dual PI3K/mTOR inhibitors demonstrate primarily superior cytostatic effects in vitro but a mixed level of cytotoxicity when compared to RAD001. In addition, the dual PI3K/mTOR inhibitors extended survival in NOD/SCID mice engrafted with ALL xenografts but failed to demonstrate overall superiority over mTOR inhibition alone. This work contributed to the publication of a paper, presented in two separate chapters. Subsequent unpublished work presented in this thesis examined the effects of the dual PI3K/mTOR inhibitors in combination with conventional chemotherapeutic agents. However, the results presented in this thesis indicate that the dual PI3K/mTOR inhibitors do not cooperate well with the tested agents. Furthermore, the cooperation observed with the dual PI3K/mTOR inhibitors in combination with a MEK inhibitor highlights the need to explore strategies to target multiple signalling pathways.
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Gulati, Ruhi. "Developing Viral Strategies to Study mTOR and its Regulators as Mediators of Epileptogenesis." University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1563273811946353.

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Payne, Sara Lauren. "Small-molecule inhibitors of mTOR and DNA-PK." Thesis, University of Newcastle Upon Tyne, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627731.

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The phosphatidylinositol-3-kinase related kinase (PIKK) family of proteins consists of five serine-threonine protein kinase members (ATM, ATR, hSMG, DNA-PK and mTOR), each of which have been implicated in the cellular response to DNA damage or cellular stress. Upregulation of the PBKJAKT cell signalling pathway has been demonstrated to be a common driver of malignancy in human cancer. The mammalian target of rapamycin (mTOR) exists in two isoforms, both of which lie within the PBKJAKT pathway and as such are capable of mediating the activity of the signalling pathway. The first reported inhibitor of mTOR was rapamycin, a macrocylic lactone which acts an allosteric inhibitor of the mTORCI complex only. Subsequent drug discovery efforts have been focussed upon the development of ATP-competitive inhibitors of mTOR, which would facilitate the inhibition of both mTOR complexes thereby interrupting the P13K/AKT pathway at two distinct points.
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Books on the topic "MTOR"

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Weichhart, Thomas, ed. mTOR. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-430-8.

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Polunovsky, Vitaly A., and Peter J. Houghton, eds. mTOR Pathway and mTOR Inhibitors in Cancer Therapy. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-271-1.

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Houghton, Peter J., and V. A. Polunovskiĭ. mTOR pathway and mTOR inhibitors in cancer therapy. New York: Humana Press, 2010.

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mTor: Methods and protocols. New York: Humana Press, 2012.

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Dey, Nandini, Pradip De, and Brian Leyland-Jones, eds. PI3K-mTOR in Cancer and Cancer Therapy. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-34211-5.

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Mita, Monica, Alain Mita, and Eric K. Rowinsky, eds. mTOR Inhibition for Cancer Therapy: Past, Present and Future. Paris: Springer Paris, 2016. http://dx.doi.org/10.1007/978-2-8178-0492-7.

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"Khorhē ew mtir--": "Tsanir zkʻez--". [S.l.]: Hratarakutʻiwn Hayk ew Ēlza Titizean Fonti, 2011.

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Transportation, Ontario Ministry of. MTO drainage management manual. [Toronto]: Ministry of Transportation, 1995.

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The official MTO driver's handbook. Ontario]: Road User Safety Division of the Ministry of Transportation of Ontario, 2013.

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Associates, R. V. Anderson, and Ontario Ministry of Transportation, eds. MTO drainage management technical guidelines. Downsview, Ont: Highway Design Office, Highway Engineering Division, Ontario Ministry of Transportation, 1989.

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Book chapters on the topic "MTOR"

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Robitaille, Aaron M. "mTOR." In Encyclopedia of Signaling Molecules, 3239–47. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_331.

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, Matthias Gaestel, Shiri Procaccia, Rony Seger, Shin Yasuda, et al. "mTOR." In Encyclopedia of Signaling Molecules, 1129–36. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_331.

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Patel, Nisha R., Michael L. Wong, Anthony E. Dragun, Stephan Mose, Bernadine R. Donahue, Jay S. Cooper, Filip T. Troicki, et al. "mTOR Inhibitors." In Encyclopedia of Radiation Oncology, 516–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_751.

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Kubica, Neil, and John Blenis. "mTORC1: A Signaling Integration Node Involved in Cell Growth." In mTOR Pathway and mTOR Inhibitors in Cancer Therapy, 1–36. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-271-1_1.

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Dowling, Ryan J. O., and Nahum Sonenberg. "Downstream of mTOR: Translational Control of Cancer." In mTOR Pathway and mTOR Inhibitors in Cancer Therapy, 201–16. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-271-1_10.

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Larsson, Ola, and Peter B. Bitterman. "Genome-Wide Analysis of Translational Control." In mTOR Pathway and mTOR Inhibitors in Cancer Therapy, 217–36. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-271-1_11.

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Bitterman, Peter B., and Vitaly A. Polunovsky. "Translational Control of Cancer: Implications for Targeted Therapy." In mTOR Pathway and mTOR Inhibitors in Cancer Therapy, 237–55. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-271-1_12.

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Pelletier, Jerry, and Jeremy R. Graff. "Downstream from mTOR: Therapeutic Approaches to Targeting the eIF4F Translation Initiation Complex." In mTOR Pathway and mTOR Inhibitors in Cancer Therapy, 257–85. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-271-1_13.

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Feng, Zhaohui, and Arnold J. Levine. "The Regulation of the IGF-1/mTOR Pathway by the p53 Tumor Suppressor Gene Functions." In mTOR Pathway and mTOR Inhibitors in Cancer Therapy, 37–48. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-271-1_2.

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Mead, Henry, Mirjana Zeremski, and Markus Guba. "mTOR Signaling in Angiogenesis." In mTOR Pathway and mTOR Inhibitors in Cancer Therapy, 49–74. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-271-1_3.

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Conference papers on the topic "MTOR"

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Rodrik-Outmezguine, Vanessa S., Masanori Okaniwa, Zhan Yao, Chris Novotny, Claire McWhirter, Arpitha Banaji, Helen Won, et al. "Abstract 2147: Overcoming mTOR resistance mutations with a new generation mTOR inhibitor." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2147.

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Pereira, Luan Filipe de Souza, KARLA FABIANE LOPES DE MELO, FRANCISCO CANINDÉ FERREIRA DE LUNA, EDNA CRISTINA SANTOS FRANCO, and SAMIR MANSOUR MORAES CASSEB. "ANÁLISE DA EXPRESSÃO DE MTOR EM TECIDOS DE FÊMEAS DA ESPÉCIE MESOCRICETUS AURATUS INFECTADOS COM O VÍRUS ZIKA." In II Congresso Brasileiro de Imunologia On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/ii-conbrai/6778.

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Introdução: Arbovírus são reconhecidos pela Organização Mundial de Saúde (OMS) como um grande problema de Saúde Pública devido à sua expansão territorial e necessidades de controle e prevenção, as quais são complexas. O vírus Zika (VZIK) está entre os arbovírus que apresentam maior circulação. Objetivo: Portanto, este estudo objetivou avaliar a expressão de mTOR em tecidos de fêmeas da espécie Mesocricetus auratus infectados com o vírus Zika. Metodologia: As amostras infectadas foram provenientes de um estudo prévio intitulado “infecção experimental do vírus Zika em Hamsters Dourados (Mesocricetus auratus), do grupo de infecções sexualmente transmissíveis, sendo aprovado previamente pelo Comitê de Ética em Pesquisa com Animais (CEUA) do Instituto Evandro Chagas (IEC), sob registro nº 24/2016. Foram um total de 63 amostras divididas entre animais infectados e não infectados. Foi realizada a extração e quantificação da carga viral, seguida por RT-qPCR. Resultados: Os tecidos de animais analisados foram cérebro de fêmea (CF), útero (UT) e cérebro de neonato. Foi realizada a quantificação da carga viral nos tecidos analisados e uma alta carga viral foi verificada com dias pós infecção (DPI) nos grupos CF e UT. Após 7 DPI foi possível verificar queda na carga viral, sendo estatisticamente significativa para CF e não estatisticamente significativa para UT. No 23º DPI foi possível verificar ausência da carga viral no grupo CF. Após a análise da carga viral, foi realizada a análise da proteína mTOR 1 e mTOR 2. mTOR 1 apresentou uma expressão positiva, enquanto que mTOR 2 apresentou uma expressão negativa. Conclusão: Este estudo demonstrou que o VZIK pode alterar as expressões de mTOR 1 e mTOR 2 de células infectadas. Sendo esta relação intimamente ligada à proliferação de macrófagos e neutrófilos durante a infecção por VZIK, assim, afetando diretamente a defesa contra esse agente viral.
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Li, Wen-ze, and De-wu Ding. "Network Analysis of mTOR Regulator." In 2012 Sixth International Conference on Internet Computing for Science and Engineering (ICICSE). IEEE, 2012. http://dx.doi.org/10.1109/icicse.2012.26.

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Yee, D., and N. J. Nassikas. "Tortured by mTOR Inhibitors? A Case of Pneumocystis Pneumonia Originally Diagnosed as mTOR Pneumonitis." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1413.

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Bezrukova, A. I., K. S. Basharova, I. V. Miliukhina, S. N. Pchelina, and T. S. Usenko. "EXPRESSION OF AUTOPHAGY-RELATED GENES IN GBA1 MUTATIONS CARRIERS WITH AND WITHOUT PARKINSON’S DISEASE." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-297.

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The molecular mechanisms of the neurodegenerative disease, Parkinson’s disease (PD), associated with mutations in the GBA1 gene (GBA-PD) are unknown. Recent data point to the role of autophagy, in particular of the PI3K/AKT/mTOR pathway, in PD pathogenesis. The study revealed pronounced alterations in the expression of autophagy-related genes are involved in the PI3K/AKT/mTOR pathway in GBA-PD. v
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Grabiner, Brian, Nikhil Wagle, Eliezer Van Allen, Levi Garraway, Jochen Lorch, and David Sabatini. "Abstract PR04: mTOR mutations in cancer." In Abstracts: AACR Special Conference: Targeting the PI3K-mTOR Network in Cancer; September 14-17, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-8514.pi3k14-pr04.

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O'Callaghan, M., M. Alquier, C. O'Brien, A. Fabre, J. Duignan, A. N. Franciosi, J. D. Dodd, M. P. Keane, D. J. Muphy, and C. Mccarthy. "Mtor Signalling and More in Dipnech." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a2244.

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Cani, Alice, Carolina Simioni, Silvano Capitani, Alberto M. Martelli, and Luca M. Neri. "Abstract 3736: The mTOR inhibitor, RAD001, displays higher cytotoxicity in leukemias with hyperactivated PI3K/AKT/mTOR pathway." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3736.

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Blanco, Elvin, Takafumi Sangai, Funda Meric-Bernstam, and Mauro Ferrari. "Chemotherapeutic Synergy Enhancement Through Micellar Nanotherapeutics." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13263.

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Current chemotherapeutic regimens involve the administration of a combination of agents with hopes of gaining synergistic cell-killing effects observed in vitro. However, drug synergy is rarely realized clinically given the different pharmacokinetic profiles of the drugs. Recent findings show that a combination of rapamycin and paclitaxel proves highly effective at hindering growth of tumors wherein the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway. Our objective was to fabricate a micellar nanotherapeutic platform capable of delivering a multitude of agents shown to synergistically affect a specific pathway (PI3K/Akt/mTOR) in breast cancer. We hypothesized that this concomitant delivery strategy will result in increased antitumor efficacy, given the site-specific and controlled delivery of the two agents. Herein, we demonstrate the successful fabrication of a nanotherepeutic strategy for the treatment of breast tumors with aberrant PI3K/Akt/mTOR pathways. Resulting polymer micelles were small in size (∼30 nm) and showed high levels of drug incorporation efficiency of both rapamycin and paclitaxel. Current studies involve the examination of release kinetics and antitumor efficacy in in vitro and in vivo models.
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Thomas, George. "Abstract PL03-07: Obesity and mTOR signaling." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Nov 7-10, 2010; Philadelphia, PA. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1940-6207.prev-10-pl03-07.

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Reports on the topic "MTOR"

1

Guan, Kun-Liang. Regulation of mTOR by Nutrients. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada569533.

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Guan, Kun-Liang. Regulation of mTOR by Nutrients. Fort Belvoir, VA: Defense Technical Information Center, July 2010. http://dx.doi.org/10.21236/ada602038.

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Ramesh, Vijaya, and Anat Stemmer-Rachamimov. Role of Merlin/NF2 in mTOR Signaling and Meningioma Growth. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada566365.

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Roberge, Michel. Study of mTOR Signaling Inhibitors as Potential Treatment for TSC. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada601809.

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Costa-Mattioli, Mauro. The Role of the New mTOR Complex, MTORC2, in Autism Spectrum Disorders. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613836.

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Barash, Itamar, and Robert Rhoads. Translational Mechanisms Governing Milk Protein Levels and Composition. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7696526.bard.

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Original objectives: The long-term goal of the research is to achieve higher protein content in the milk of ruminants by modulating the translational apparatus of the mammary gland genetically, nutritionally, or pharmacologically. The short-term objectives are to obtain a better understanding of 1) the role of amino acids (AA) as regulators of translation in bovine and mouse mammary epithelial cells and 2) the mechanism responsible for the synergistic enhancement of milk-protein mRNA polyadenylation by insulin and prolactin. Background of the topic: In many cell types and tissues, individual AA affect a signaling pathway which parallels the insulin pathway to modulate rates and levels of protein synthesis. Diverse nutritional and hormonal conditions are funneled to mTOR, a multidomain serine/threonine kinase that regulates a number of components in the initiation and elongation stages of translation. The mechanism by which AA signal mTOR is largely unknown. During the current grant period, we have studied the effect of essential AA on mechanisms involved in protein synthesis in differentiated mammary epithelial cells cultured under lactogenic conditions. We also studied lactogenic hormone regulation of milk protein synthesis in differentiated mammary epithelial cells. In the first BARD grant (2000-03), we discovered a novel mechanism for mRNA-specific hormone-regulated translation, namely, that the combination of insulin plus prolactin causes cytoplasmic polyadenylation of milk protein mRNAs, which leads to their efficient translation. In the current BARD grant, we have pursued the signaling pathways of this novel hormone action. Major conclusions/solutions/achievements: The positive and negative signaling from AA to the mTOR pathway, combined with modulation of insulin sensitization, mediates the synthesis rates of total and specific milk proteins in mammary epithelial cells. The current in vitro study revealed cryptic negative effects of Lys, His, and Thr on cellular mechanisms regulating translation initiation and protein synthesis in mammary epithelial cells that could not be detected by conventional in vivo analyses. We also showed that a signaling pathway involving Jak2 and Stat5, previously shown to lead from the prolactin receptor to transcription of milk protein genes, is also used for cytoplasmic polyadenylation of milk protein mRNAs, thereby stabilizing these mRNAs and activating them for translation. Implications: In vivo, plasma AA levels are affected by nutritional and hormonal effects as well as by conditions of exercise and stress. The amplitude in plasma AA levels resembles that applied in the current in vitro study. Thus, by changing plasma AA levels in the epithelial cell microenvironment or by sensitizing the mTOR pathway to their presence, it should be possible to modulate the rate of milk protein synthesis. Furthermore, knowledge that phosphorylation of Stat5 is required for enhanced milk protein synthesis in response to lactogenic opens the possibility for pharmacologic approaches to increase the phosphorylation of Stat5 and, thereby, milk protein production.
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Yu, Kyung, Latha Narayanan, John Schlager, Jeffery Gearhart, and Peter Robinson. Kinetic Behavior of Leucine and Other Amino Acids Modulating Cognitive Performance via mTOR Pathway. Fort Belvoir, VA: Defense Technical Information Center, December 2011. http://dx.doi.org/10.21236/ada560396.

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Ellis, Leigh. Inhibition of Histone Deacetylases (HDACs) and mTOR Signaling: Novel Strategies Towards the Treatment of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada562460.

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Jongens, Thomas A. Examination of the mGluR-mTOR Pathway for the Identification of Potential Therapeutic Targets to Treat Fragile X. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada612771.

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Su, Bing. The Role of mTOR Signaling in the Regulation of RAG Expression and Genomic Stability during B Lymphocyte Development. Fort Belvoir, VA: Defense Technical Information Center, May 2013. http://dx.doi.org/10.21236/ada588301.

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