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Dissertations / Theses on the topic 'MTOR'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

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

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2

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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3

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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4

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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5

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 con

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6

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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7

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<br>Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas<br>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<br>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 mec

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8

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 presente

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9

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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10

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 inhibi

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11

Peter, Christian. "mTOR signalling and the regulation of FOXP3 expression." Thesis, University of Oxford, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.600239.

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Regulatory T-cells (Treg) are essential for the establishment of self-tolerance and they can be identified by the expression of FOXP3, the "master" transcription factor for the development of Treg. A number of essential Signals, namely TCR engagement, TGF~, as well as the inhibition of the kinase mTOR, have been shown to be crucial for the induction of FOXP3 in the peripheral immune system. Despite recent progress, the molecular mechanisms for induction of FOXP3 remains elusive due, at least in part, to the lack of a cell line that mimics the behavior of primary CD4+ T-cells. Here we report th

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12

Graham, Emma Louise. "The regulation of Pol III transcription by mTOR." Thesis, University of Glasgow, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414344.

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13

Morris, Katherine Louise. "Investigation of RNA binding proteins regulated by mTOR." Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/39742.

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The mammalian target of rapamycin (mTOR) is a serine/threonine protein kinase which plays a key role in the transduction of cellular energy signals, in order to coordinate and regulate a wide number of processes including cell growth and proliferation via control of protein synthesis and protein degradation. For a number of human diseases where mTOR signalling is dysregulated, including cancer, the clinical relevance of mTOR inhibitors is clear. However, understanding of the mechanisms by which mTOR controls gene expression is incomplete, with implications for adverse toxicological effects of

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14

Alharbi, Z. M. S. "Identification and characterization of novel mTOR splicing isoforms." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1459435/.

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mTOR (mammalian target of rapamycin) is a serine/threonine protein kinase which belongs to the family of phosphoinositide 3-kinase related kinases (PIKK), which also includes ATR, ATM, DNA-PK, SMG1 and TRRAP. mTOR contains several conserved protein-protein interaction modules at the N-terminus and a protein kinase domain at the C-terminus. The regulatory interactions of mTOR are mainly mediated by HEAT (Huntingtin, Elongation factor 3, protein phosphatase 2A, and TOR1) repeats and FAT (FRAP, ATM and TRRAP) domains. In contrast to other PIKK family members, mTOR possesses a unique FRB (FKBP12/R

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15

Earwaker, Philip L. "Resistance mechanisms to mTOR inhibition in renal cancer." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:dc500011-d486-43cc-a0a7-87b9d6d9e682.

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<b>Introduction</b>: Advanced clear cell renal cell cancer (CCRCC) is incurable, but molecularly targeted treatments have improved the prognosis. One such molecular target is the mammalian target of rapamycin (mTOR) and two rapalogues (everolimus and temsirolimus) have been licensed for the treatment of advanced CCRCC, but resistance to treatment is a significant problem. Novel mTOR kinase inhibitors show more complete blockade of mTOR downstream targets, and greater in vitro anti proliferative activity, although resistance remains a problem. <b>Hypotheses</b>: 1) CCRCC cell lines, resistant t

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16

Hare, Stephen. "The development and characterisation of everolimus resistant breast cancer cells." Thesis, Brunel University, 2018. http://bura.brunel.ac.uk/handle/2438/17466.

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The mTOR inhibitor and rapalogue everolimus was approved use in 2012, in HR+, HER-2-, post-menopausal patients, who had previously failed aromatase inhibitor treatment. mTOR pathway activation has been associated with resistance to breast cancer therapies, but how cells may become resistant to mTOR therapies themselves in breast cancer is currently not well explored, due to the relative recentness of everolimus approval. Drug resistance across all areas of cancer research is a major clinical issue, often leading to the spread of a patient's cancer. This project set out to create in vitro breas

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17

Suárez, Rodríguez Cristina. "Valor pronóstico de las alteraciones genéticas de la vía mTOR en pacientes con cáncer renal metastásico tratados con inhibidores de mTOR." Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/664121.

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El cáncer renal supone el 2% de todos los nuevos casos de cáncer en el adulto y su incidencia va en aumento en los últimos años. El mejor conocimiento de la biología molecular del cáncer renal ha llevado al descubrimiento y utilización de dos grandes grupos de fármacos: los inhibidores de la vía de la angiogénesis y los inhibidores de la vía mTOR, a los que recientemente se ha unido la inmunoterapia. Existen dos inhibidores de mTOR (imTOR) aprobados en el tratamiento de cáncer renal: temsirolimus y everolimus. Diversos estudios han demostrado que las alteraciones genéticas en la vía mTOR

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18

Schollenberger, Daniel [Verfasser]. "Immunhistochemische Analyse der Expressionsniveaus von mTOR und p-mTOR in Metastasen von Nierenzellkarzinomen unter der Berücksichtigung ihrer prognostischen Relevanz / Daniel Schollenberger." Tübingen : Universitätsbibliothek Tübingen, 2021. http://d-nb.info/1230796495/34.

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19

Silva, Hamilton Augusto Roschel da. "Efeito agudo de diferentes velocidades de exercício excêntrico na sinalização da hipertrofia muscular." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/39/39132/tde-22062012-103944/.

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Atualmente, alguns pesquisadores tem se dedicado ao estudo do efeito da manipulação do treinamento de força sobre a ativação das vias de sinalização intracelular para hipertrofia. Tem-se sugerido que o grau de tensão muscular desempenhe um papel importante nesta sinalização. Dentre os diferentes tipos de ações musculares, as ações excêntricas (AE) reconhecidamente proporcionam maior grau de tensão à estrutura do músculo esquelético. Em particular, AE de alta velocidade parecem exercer um efeito interessante sobre os ganhos de hipertrofia muscular. Porém, pouco se sabe sobre o efeito da manipul

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20

Alqurashi, Naif. "The Therapeutic Potential of mTOR signalling Pathway as Drug Target in Human Colorectal Cancer." Thesis, Griffith University, 2015. http://hdl.handle.net/10072/367346.

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The mammalian target of rapamycin (mTOR), a downstream effector of PI3K/Akt signalling, is a critical regulator of cellular processes in response to oncogenic signals. In mammalian cells, mTOR exists in 2 large physically and functionally distinct signalling complexes, i.e.: mTORC1 and mTORC2. Each complex has its own set of downstream targets, which modulate cellular growth, proliferation, and survival in normal cells and cancer. Deregulation of mTOR signalling often occurs in a variety of human malignant diseases, making it a validated target in the development of treatments for cancer. In c

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21

Houssaini, Amal. "La voie de signalisation Akt/mTOR : rôle physiopathologique etcible thérapeutique dans l’hypertension artérielle pulmonaire expérimentale." Thesis, Paris Est, 2012. http://www.theses.fr/2012PEST0069.

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Les travaux de la thèse portent sur l'implication de la voie de signalisation Akt (sérine/thréonine kinase Akt) et mTOR (mammalian target of rapamycin) dans la physiopathologie de l'hypertension artérielle pulmonaire (HTAP) expérimentale. L'HTAP résulte d'une prolifération exagérée des cellules constitutives des vaisseaux pulmonaires, principalement les cellules musculaires lisses artérielles pulmonaires (CML-AP). De nombreux effecteurs biologiques et physiques préalablement identifiés agissent sur les CML-AP et participent à l'hyperplasie de celles-ci. Nous montrons que ces nombreux effecteur

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22

Boudra, Rafik. "Rôle de la Nucléophosmine (NPM1) dans la physiopathologie prostatique." Thesis, Clermont-Ferrand 2, 2015. http://www.theses.fr/2015CLF22598/document.

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La Nucléophosmine (NPM1/B23) est une petite chaperonne moléculaire impliquée dans de nombreux processus cellulaires, tels que la régulation de l’expression génique ou le contrôle du cycle cellulaire. De nombreuses études rapportent une surexpression de NPM1 dans divers types de tumeurs solides incluant les cancers de la prostate, et son rôle proH prolifératif dans des lignées cellulaires tumorales d’origines variées est bien établi. La première partie de notre travail s’est attaché à évaluer le potentiel oncogénique de NPM1 dans l’épithélium prostatique in vivo. Pour cela, nous avons généré un

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23

Kalender, Adem. "Regulation of the mTOR/S6K pathway by cellular energy /." [S.l.] : [s.n.], 2009. http://edoc.unibas.ch/diss/DissB_8784.

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24

Seymour, Lyndsey A. "Characterising the signalling mechanism of the mTOR-dependent phosphatase." Thesis, Cardiff University, 2011. http://orca.cf.ac.uk/55115/.

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The mechanistic Target of Rapamycin Complex 1 (mTORC1) complex is central in the regulation of many crucial cellular processes including translation, transcription, proliferation and autophagy. Deregulation of the complex is evident in a number of diseases including Tuberous Sclerosis, Alzheimer's Disease and cancer. Whilst the signalling events leading to activation of mTORC1 are well understood, the inhibitory phosphatase activity that prevents aberrant signalling has received comparatively little attention. In yeast, phosphatases are an integral part of TORC1 signalling. Poor nitrogen suppl

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25

Sully, Katherine L. "Inhibition of mammalian target of rapamycin (mTOR) in epidermis." Thesis, Queen Mary, University of London, 2012. http://qmro.qmul.ac.uk/xmlui/handle/123456789/3360.

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Cutaneous squamous cell carcinoma (cSCC) is one of the most common Caucasian skin cancers and is particularly prevalent following chronic ultraviolet (UV) radiation exposure and in immunosuppressed patients. Recent use of rapamycin as an immunosuppressant significantly reduces SCC after organ transplantation. However the mechanism remains unclear. Rapamycin inhibits mammalian target of rapamycin (mTOR) kinase, downstream from phosphatidylinositol-3 kinase (PI3K) and Akt kinases previously implicated in SCC. The aim was to find the effects of rapamycin on PI3K-Akt-mTOR signalling in epidermis i

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26

Kawashima, Naomasa. "The interaction of mTOR and autophagy in salivary glands." Thesis, King's College London (University of London), 2018. https://kclpure.kcl.ac.uk/portal/en/theses/the-interaction-of-mtor-and-autophagy-in-salivary-glands(a5382fc9-c83b-4046-bff4-98c1b4ed91c5).html.

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Radiation therapy to treat head and neck cancer damages salivary glands, leading to decreased salivary flow which can cause xerostomia (perception of dry mouth), mucositis and dysphagia. These symptoms of salivary gland hypofunction are a major cause of patients stopping their treatment and greatly decrease their quality of life after treatment. Protecting from damage is essential to avoid these problems so this thesis examined some of the damage mechanisms present in salivary glands. Two intracellular processes seem to be particularly relevant. Mammalian Target of Rapamycin (mTOR) is a growth

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27

Pereira, Carla Sofia Domingues. "Via de sinalização mTOR no carcinoma urotelial da bexiga." Master's thesis, [s.n.], 2014. http://hdl.handle.net/10284/4673.

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Trabalho de Projeto apresentado à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Mestre em Análises Laboratoriais Especializadas, área de especialização em Análise Biomédica<br>Mundialmente, o cancro da bexiga (CB) é o 7º tipo de cancro mais frequente em homens e o 17 º mais frequente em mulheres. É uma doença com etiologia multifatorial associada a vários agentes ambientais e genéticos, dos quais o tabagismo é o fator de risco mais importante. Os carcinomas uroteliais da bexiga (CUBs) são geralmente superficiais em 70% a 80% dos pacientes e invasores em 20% a

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Mota, Filipa Dias Alves da. "Carcinoma urotelial da bexiga e via de sinalização mTOR." Master's thesis, [s.n.], 2012. http://hdl.handle.net/10284/3742.

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Projeto de Pós-Graduação/Dissertação apresentado à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Mestre em Ciências Farmacêuticas<br>O carcinoma da bexiga é o quinto tumor maligno mais comum, representando cerca de 3,2% de todos os cancros no mundo. A sua patogénese envolve alterações genéticas somáticas induzidas por agentes carcinogéneos ambientais, tais como o tabaco, as aminas aromáticas ou o arsénio. Apesar da caracterização elaborada dos fatores de risco, o carcinoma da bexiga ainda é um problema epidemiológico importante, cuja incidência continua a aume

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29

Bozorgi, Sophie Shaghayegh. "Role of mTOR in salivary gland atrophy and regeneration." Thesis, King's College London (University of London), 2016. https://kclpure.kcl.ac.uk/portal/en/theses/role-of-mtor-in-salivary-gland-atrophy-and-regeneration(261e1f87-673f-498e-891b-3f57395c04ff).html.

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The mammalian target of rapamycin (mTOR) is a protein kinase whose dysfunction has been identified in many diseases ranging from cancer to Down’s syndrome. Previous studies have examined salivary gland atrophy and observed the submandibular gland’s ability to regenerate from atrophy, however the mechanism underlying this process is still unknown. The current study aims to investigate the effects of blocking mTOR signaling in atrophic salivary glands and blocking mTOR signalling in submandibular glands regenerating from atrophy. The first part of the study revealed that inhibition of mTOR delay

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30

Obayashi, Yoko. "Novel physiological function of proline and mTOR regulator tuberin." Kyoto University, 2018. http://hdl.handle.net/2433/232154.

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31

Jobim, Paulo Fernandes Costa. "Papel de mTOR na formação e reconsolidação da memória." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2011. http://hdl.handle.net/10183/35905.

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Novas informações assimiladas pelo sistema nervoso primeiramente ficam em um estado de labilidade para depois se estabilizarem através de um processo conhecido como consolidação, que envolve síntese de proteínas. Depois da reativação, uma memória previamente consolidada retorna ao seu estado de labilidade, e para que volte a ser estável, é necessário que haja novamente síntese de proteínas. Este segundo processo é chamado de reconsolidação. Recentemente os mecanismos moleculares e celulares envolvidos na regulação da síntese protéica relacionados à formação de memória de longa duração vêm send

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Mushaben, Elizabeth M. "BMPR2 and mTOR Signaling Pathways in Inflammatory Lung Diseases." University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1352485302.

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KHAPRE, ROHINI VISHAL. "CIRCADIAN REGULATION OF mTOR SIGNALING VIA BMAL1 DEPENDENT MECHANISM." Cleveland State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=csu1399025275.

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34

Pothiraju, Deepika [Verfasser]. "Targeting PI3K/mTOR pathway in hepatocellular carcinoma / Deepika Pothiraju." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover (TIB), 2011. http://d-nb.info/1013286243/34.

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35

Caccamo, Antonella Maria Giovanna. "The role of mTOR signaling in Alzheimer s disease." Doctoral thesis, Università di Catania, 2016. http://hdl.handle.net/10761/3767.

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The majority (>95%) of Alzheimer s disease (AD) cases are sporadic and of unknown causes. The single major risk factor for AD is aging and molecular changes that occur in the brain as a function of age may facilitate the development of AD. However, little is known as to how the aging process facilitates the development of AD. Overwhelming evidence shows that reducing the activity of the mammalian target of rapamycin (mTOR) increases lifespan and health-span in several genetically different species. mTOR is a ubiquitously expressed protein kinase that plays a key role in regulating protei

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Machado, Camila de Oliveira Freitas. "Estudo do envolvimento da proteína colibistina no controle do início da tradução." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/41/41131/tde-15122014-142323/.

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A proteína colibistina (CB), uma Rho GEF neuro-especifica, apresenta papel importante na formação e funcionamento das sinapses inibitórias do sistema nervoso central por interagir com a proteína scaffold gefirina e com receptores GABAA e promover o agrupamento e transporte dessas proteínas para a membrana pós-sináptica. Recentemente, nosso grupo de pesquisa identificou interação de CB com um complexo proteico que controla o início da tradução em eucariotos (complexo eIF3), o que sugeriu pela primeira vez que essa proteína pode estar envolvida também na regulação da tradução em células neurais.

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Rocha, Alisson Luiz da. "Overreaching não funcional em modelo animal: adaptações inflamatórias e hipertróficas do músculo cardíaco." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17152/tde-23032018-134837/.

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O overreaching não funcional (NFOR) induzido pelo exercício excêntrico (EE) em modelo animal está associado com a diminuição de desempenho físico, dano no DNA (amostras de músculo esquelético e soro), estresse oxidativo (amostras de músculo esquelético e soro), inflamação crônica de baixo grau (amostras de músculo esquelético e soro) e prejuízo da via de sinalização da insulina (amostras de músculo esquelético). No entanto, as adaptações do músculo cardíaco em resposta ao estado de NFOR induzido ou não pela predominância do EE ainda não foram investigadas. Além disso, sabe-se que a mTOR (mamma

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38

Reita, Damien. "Evaluation préclinique d'une nouvelle combinaison thérapeutique associant l'irinotécan à un inhibiteur de mTOR pour le traitement des tumeurs coliques." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ071.

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Positionnée en aval des voies PI3K/AKT et RAS/MAPK, la protéine kinase mTOR joue un rôle déterminant dans le développement et la progression tumorale des cancers colorectaux où elle est fortement surexprimée. Par ailleurs, les cancers colorectaux comme toutes les tumeurs solides, ont un microenvironnement hypoxique. L’adaptation des cellules tumorales à l’hypoxie est notamment régulée par la voie PI3K/AKT/mTOR ainsi que par les facteurs de transcription HIFs dont l’expression protéique et l’activité transcriptionnelle est en partie régulée par mTOR. Dans cette étude, nous avons montré que l’in

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Vicier, Cecile. "Implication de la pseudokinase dans la réponse aux inhibiteurs de mTor." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS320.

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MTor est une protéine centrale de la voie de signalisation PI3K/AKT/mTor et est impliquée dans la croissance, la prolifération et la survie cellulaire. Cette protéine joue un rôle majeur particulièrement dans la prolifération tumorale. Ainsi des inhibiteurs de mTor ont été développés à partir des années 1980, notamment la rapamycine, et deux sont utilisés actuellement en clinique: l’évérolimus et le temsirolimus. Ces deux inhibiteurs font partie des différentes possibilités thérapeutiques dans les cancers du sein et du rein métastatiques. Les patients traités présentent des réponses variées av

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40

Nierhoff, Ann-Kathrin [Verfasser], and Hagen Sjard [Akademischer Betreuer] Bachmann. "Bedeutung von genetischen Polymorphismen im MTOR-Gen bei Patienten nach Nierentransplantation unter und ohne mTOR-Inhibitor-Therapie / Ann-Kathrin Nierhoff ; Betreuer: Hagen Sjard Bachmann." Duisburg, 2019. http://d-nb.info/1191690873/34.

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Kellenberger, Antonia Judit [Verfasser], and Elke [Akademischer Betreuer] Lütjen-Drecoll. "Die Beteiligung von mTOR an der Regulation des Haarzyklus und Einfluss von Bimatoprost auf die mTOR Aktivierung / Antonia Judit Kellenberger. Betreuer: Elke Lütjen-Drecoll." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2011. http://d-nb.info/1056066474/34.

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Moorthy, Ganesh. "Clinical Pharmacokinetics of the Novel Combination of BEZ235, PI3K/mTOR Inhibitor, and Everolimus, mTOR Inhibitor: Phase I Clinical Studies and Non-clinical Mechanistic Assessment." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1439296033.

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Silva, Adriana Caldo. "Efeitos do overreaching não funcional sobre a via da mTOR no tecido hepático de camundongos." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/17/17152/tde-04012017-113714/.

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O propósito do presente estudo foi verificar os efeitos do overtraining (OT) nas proteínas relacionadas com a via de sinalização da mammalian target of the rapamycin complex 1 (mTORC1), no conteúdo proteico de sterol regulatory element binding protein-1 (SREBP-1) e nas características morfológicas do fígado de camundongos C57BL/6. Os animais foram divididos em grupo controle (CT), overtraining em declive (OTR/down), overtraining em aclive (OTR/up) e overtraining sem inclinação (OTR). Teste do rotarod, incremental, exaustivo e força de preensão foram utilizados para avaliação de performance. Ap

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Dowling, Ryan. "The role of mTOR signalling in translational control and cancer." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66869.

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Abstract The serine/threonine kinase mTOR plays a critical role in the regulation of cellular proliferation, growth, differentiation, autophagy, and cytoskeletal organization. Two mTOR containing complexes exist in mammalian cells: mTORC1 and mTORC2. mTORC1 mediates its effects through the control of mRNA translation initiation via phosphorylation of its two major downstream targets: the 4E-BPs and S6Ks. In order to study the individual roles of S6Ks and 4E-BPs downstream of mTORC1, we utilized new active-site mTOR inhibitors and cells deficient for either 4E-BPs or S6Ks. Sur

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Kaeuferle, Theresa. "Identification of microRNAs regulating adipocyte differentiation via mTOR nutrient-signaling." Diss., Ludwig-Maximilians-Universität München, 2015. http://nbn-resolving.de/urn:nbn:de:bvb:19-182836.

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Tam, Ka-ho Chris, and 譚家豪. "Targeting mTOR as a novel therapeutic strategy for hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B41508476.

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Carvalho, Lucas de Lima. "InibiÃÃo do mTOR agrava a mucosite intestinal induzida por irinotecano." Universidade Federal do CearÃ, 2016. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=18610.

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Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico<br>INTRODUÃÃO. O cÃncer colorretal (CCR) Ã uma das neoplasias mais prevalentes em todo o mundo, sendo uma das principais causas de Ãbito por cÃncer. No Brasil, apresenta-se como o terceiro cÃncer mais frequente nos homens e segundo nas mulheres. Nas Ãltimas dÃcadas novas drogas incorporadas Ã protocolos clÃnicos para o tratamento do CCRm tem proporcionado um aumento significativo na sobrevida de pacientes com esse tipo de malignidade. Dentre estas drogas o irinotecano ocupa lugar de destaque e Ã comumente utilizado como primeira lin

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Abelaira, Helena Mendes. "O papel da via mTOR no efeito antidepressivo da cetamina." reponame:Repositório Institucional da UNESC, 2017. http://repositorio.unesc.net/handle/1/5002.

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Tese apresentada ao Programa de Pós-Graduação em Ciências da Saúde da Universidade do Extremo Sul Catarinense - UNESC, como requisito parcial para a obtenção do título de Doutor em Ciências da Saúde.<br>Estudos recentes indicam que a via de sinalização da proteína alvo da rapamicina em mamíferos (mTOR) está relacionada com a fisiopatologia do transtorno depressivo maior (TDM). A cetamina, um antagonista do receptor N-metil-D-asparto (NMDA), foi identificada como uma nova terapia para o TDM, no entanto, o seu mecanismo de ação como antidepressivo não é ainda totalmente compreendido. Evidências

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Market, Marisa Rae. "TGFβ Causes Postoperative Natural Killer Cell Paralysis Through mTOR Inhibition". Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/40945.

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Background: Life-prolonging tumour removal surgery is associated with increased metastasis and disease recurrence. Natural Killer (NK) cells are critical for the anti-tumour immune response. Postoperatively, NK cell cytotoxicity and interferon-gamma (IFNγ) production are profoundly suppressed and this dysfunction has been linked to increased metastases/poor patient outcomes. NK cell activity depends on the integration of signals through receptors and can be modulated by soluble factors, including transforming growth factor- beta (TGFβ). The postoperative period is characterized by the expansio

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Rato, Leila Sofia Coelho. "Vimentin interacts with the Akt/mTOR pathway mediating cell growth." Master's thesis, Universidade de Aveiro, 2017. http://hdl.handle.net/10773/22372.

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Mestrado em Bioquímica - Bioquímica Clínica<br>A vimentina é uma proteína da classe III dos filamentos intermédios que promove processos tais como proliferação, migração e invasão celular através da interação com diferentes vias de sinalização. No entanto, o papel da vimentina no crescimento celular é ainda pouco conhecido. Neste estudo, observamos que fibroblastos isolados de embriões de ratinhos sem vimentina (Vim -/- MEFs) eram mais pequenos que o tipo normal (WT). Assim, o objetivo deste estudo era entender de que forma a vimentina regula o crescimento celular. Com recurso a modelos in vit

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