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Dissertations / Theses on the topic 'PI3K'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Balakrishnan, Sanjeevi. "Establishing a biological role for class II phosphoinositide 3-kinase (PI3K) enzyme PI3K-C2??" Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/39135.

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Phosphoinositide 3-Kinase (PI3K) enzymes control a variety of cellular processes and their deregulation has been extensively investigated in disease conditions including renal disease, autoimmunity and chronic inflammation. Whilst PI3K enzymes have been the subject of intense research activity, the precise biological role of PI3K-C2?? enzyme remains unclear. PI3K-C2??-/- mice developed focal segmental glomerulosclerosis, damaging podocyte morphology and affecting function. My thesis explored the contribution of the PI3K-C2?? enzyme in the pathology of chronic diseases. PI3K-C2??flx/+ mice were

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2

Hale, Benjamin G. "Influenza A viruses and PI3K signalling." Thesis, University of St Andrews, 2007. http://hdl.handle.net/10023/483.

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The influenza A virus non-structural (NS1) protein is multifunctional, and during virus-infection NS1 interacts with several factors in order to manipulate host-cell processes. This study reports that NS1 binds directly to p85β, a regulatory subunit of phosphoinositide 3-kinase (PI3K), but not to the related p85α. Expression of NS1 was sufficient to activate PI3K and cause the phosphorylation of a downstream mediator of PI3K signalling, Akt. However, in virus-infected MDCK cells, the kinetics of Akt phosphorylation did not correlate with NS1 expression, and suggested that negative regulation o

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Hale, Benjamin G. "Influenza A viruses and PI3K signalling /." St Andrews, 2008. http://hdl.handle.net/10023/483.

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4

White, Angela R. "Shared PI3K signaling abnormalities in brain tumors and epilepsy: PI3K inhibition in PTEN-deficient disorders of the brain." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1603712831970142.

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5

Castel, Morales Pau. "Molecular mechanisms of resistance to PI3K inhibitors." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/396640.

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The development of high-throughput sequencing technologies has prompted the evaluation of large cohorts of different tumor types. The results from these comprehensive genomic studies have revealed the most commonly mutated genes across human cancers, providing further understanding of the pathogenesis, molecular classification, and therapeutic strategies for this disease. PIK3CA, the gene encoding the PI3Kα isoform, is among the most frequently mutated genes in breast, head and neck, colorectal, and lung cancer, among others. Activating mutations in PIK3CA promote hyperactivation of the PI3

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6

Figueiredo, Ana Raquel Martins. "Role of PI3K in pericytes during angiogenesis." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/404276.

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Pericytes (PCs) are important regulators of the vascular development promoting vessel growth and stabilization. They have recently emerged as a therapeutic target to promote or inhibit angiogenesis. Therefore, advancing our basic understanding on PCs biology and its molecular regulators during physiological angiogenesis is essential to develop PC-related therapies. One of the major pathways leading to cellular proliferation, migration, and survival is relayed by PI3K. Data from our laboratory and others have demonstrated isoform selectivity stimulating PI3K signalling in the regulation of both

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7

Fedrigo, Carlos Alexandre. "Inibição da via PI3K-Akt em gliomas." Pontifícia Universidade Católica do Rio Grande do Sul, 2012. http://hdl.handle.net/10923/4518.

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Made available in DSpace on 2013-08-07T19:05:17Z (GMT). No. of bitstreams: 1 000439149-Texto+Completo-0.pdf: 1490829 bytes, checksum: bd616615ee5265db0a960d6f77c8581d (MD5) Previous issue date: 2012<br>Glioblastoma multiforme (GMB) is the most malignant and common type of all astrocytic tumours. Current standard treatment for GBM patients involves maximum surgical resection of the tumour, followed by radiotherapy and chemotherapy, usually containing the alkylating agent Temozolomide (TMZ). Despite this aggressive combination therapy, the survival rate of GBM patients is still low. This work

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8

Ramos, Delgado Carmen Fernanda. "Exploring PI3K signalling dynamics in pancreatic cancer." Thesis, Toulouse 3, 2020. http://www.theses.fr/2020TOU30152.

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Les PI3K sont des enzymes qui phosphorylent le groupe hydroxyl en position 3 des phosphatidylinositols comme le PIP2 ou le PI. Ces lipides sont impliqués dans de nombreux processus cellulaires tels que la croissance, la prolifération, la motilité, l'autophagie et le trafic cellulaire. Chez les mammifères, il y a 8 isoformes de PI3K et elles sont regroupées en trois classes (I, II et III) en fonction de leur structure et spécificité du substrat. Les PI3K de classe I sont les mieux caractérisées et impliquées dans le cancer. Les rôles oncogéniques des PI3K de classe II et III restent méconnus. L

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9

Karnes, Jonathan Burgess. "PI3K Class IIalpha Is Required for Autophagy." Thesis, Van Andel Research Institute, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10268645.

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<p> Autophagy is a cellular recycling process in which cytoplasmic proteins and organelles are sequestered in a double membrane vesicle, delivered to the lysosome, and degraded following fusion of the two vesicles. A key part of the initiation signaling for autophagy is the generation of phosphoinositol 3-phosphate (P13P) by class III phosphoinositol 3-kinase also knows as Vps 34. In humans there are eight P13K isoforms divided into three classes, four class I enzymes, three class II enzymes, and a single class III enzyme. Of these eight enzymes, only the class III isoform is thought to partic

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10

Zunder, Eli Richard. "A yeast screen for PI3K inhibitor resistance." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2009. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3339211.

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11

Rampanarivo, Hariniaina. "Contrôle du signal apoptotique CD95 par la voie PI3K / AKT et caractérisation de nouveaux inhibiteurs de PI3Ks." Rennes 1, 2012. http://www.theses.fr/2012REN1S086.

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Le récepteur CD95 appartient à la famille du récepteur au TNF. Son ligand, le CD95L retrouvé à la surface des cellules NK et des lymphocytes T activés, joue un rôle dans l'élimination des cellules infectées et cancéreuses. La liaison CD95L/CD95, entraîne le recrutement de FADD, qui fixe les procaspases-8/-10, pour former le DISC, nécessaire à l'induction du signal de mort. Selon la transmission du signal apoptotique CD95, 2 types cellulaires existent: les type I forment le DISC efficacement et les type II forment un DISC inefficace. Ce signal CD95 est modulé par la distribution ou l'exclusion

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12

Shibuya, Hideyuki. "TNFα, PDGF and TGFβ synergistically induce synovial lining hyperplasia via inducible PI3Kδ". Kyoto University, 2015. http://hdl.handle.net/2433/199195.

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13

Killip, Marian J. "RNA virus modulation of IFN, PI3K and apoptosis." Thesis, St Andrews, 2009. http://hdl.handle.net/10023/777.

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14

Marshall, Andrew James. "The development of PI3K inhibitors as anticancer drugs." Thesis, University of Auckland, 2010. http://hdl.handle.net/2292/6440.

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Phosphatidylinositol 3-kinases (PI3Ks) are a lipid enzyme family that are vitally important regulators of intracellular signalling pathways which control cellular activities including cell survival, growth and proliferation. Deregulation of the PI3K signalling cascade has been observed in a broad range of human diseases including cancer, diabetes, thrombosis, immunity and inflammatory disorders. With the discovery of PI3K’s link to a variety of diseases, there has been a race to produce ATP competitive inhibitors as therapeutic agents against the Class I PI3K isozymes. Herein, compounds from t

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15

Patton, Daniel Timothy. "The role of PI3K p110δ in T cells". Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612110.

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16

Fedrigo, Carlos Alexandre. "Inibi??o da via PI3K-Akt em gliomas." Pontif?cia Universidade Cat?lica do Rio Grande do Sul, 2012. http://tede2.pucrs.br/tede2/handle/tede/1696.

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Made available in DSpace on 2015-04-14T13:35:33Z (GMT). No. of bitstreams: 1 439149.pdf: 1490829 bytes, checksum: bd616615ee5265db0a960d6f77c8581d (MD5) Previous issue date: 2012-05-29<br>Glioblastoma multiforme (GMB) is the most malignant and common type of all astrocytic tumours. Current standard treatment for GBM patients involves maximum surgical resection of the tumour, followed by radiotherapy and chemotherapy, usually containing the alkylating agent Temozolomide (TMZ). Despite this aggressive combination therapy, the survival rate of GBM patients is still low. This work consisted in i

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17

López, Fauqued Marta. "Preclinical Study of PI3K and BRAF Inhibitors in Malignant Melanoma / Estudio preclínico de inhibidores de PI3K y BRAF en melanoma maligno." Doctoral thesis, Universitat de Barcelona, 2010. http://hdl.handle.net/10803/1040.

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Malignant melanoma is the most lethal skin cancer with no effective therapeutic treatment in its metastatic stages. RAS and PI3K pathways have been shown to play a critical role in melanoma development and progression. In this study, we assessed the in vitro and in vivo inhibition potential of a BRAF inhibitor (Sorafenib, Bayer) and a PI3K/mTOR inhibitor (PI-103, PIramed-Genentech) in primary melanoma cell lines. We used primary cell lines isolated from spontaneous melanomas obtained in the UV induced HGF transgenic melanoma mouse model.<br/><br/>Although PI-103 and sorafenib inhibited melanom

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18

Duarte, Andressa. "Participação da via PI3K/AKT na produção de óxido nítrico por macrófagos peritoneais." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/17/17147/tde-21102013-112320/.

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A imunidade inata é responsável pela resposta inicial aos microrganismos, uma vez que impede, controla ou elimina a infecção. Esse sistema consiste em barreiras epiteliais, proteínas plasmáticas e células circulantes e teciduais. Dentre esses componentes, os macrófagos possuem grande importância, sendo capazes de controlar e eliminar agentes patogênicos através da fagocitose e produção de espécies reativas de oxigênio e nitrogênio. A ativação de PRRs por constituintes oriundos dos patógenos em macrófagos desencadeia eventos da resposta imune inata, ativados por diversas vias de sinalização int

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19

Chu, Ying Ying Julia. "Apoptosis is promoted by unconventional FcγR-PI3KCdc42-Pak-Mek-Erk signalling in the human neutrophil". Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28813.

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Neutrophils form a first line of defence against infections. These short-lived, terminally differentiated cells perform many important functions, including chemotaxis, degranulation, reactive oxygen species (ROS) release and cytokine production. Whilst neutrophils are essential for host immunity, their inappropriate recruitment, activation and/or removal can contribute to excessive inflammation and host damage, as exemplified in autoimmune diseases such as rheumatoid arthritis. It is therefore essential that neutrophil function is tightly regulated. Neutrophils are activated by a range of stim

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20

Ma, Kewei. "Investigation of the phosphatidylinositol 3-kinase pathway in B cells." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/3818.

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There is hardly a cellular process that is not regulated in some way by phosphoinositides, which makes biochemical and physiological studies of these lipids extremely important. PI 3-kinases are key regulators of phosphoinositide metabolism and have been shown to affect a large variety of cellular responses. The key products of PI 3-kinases that have functional activity in higher eukaryotic cells are PI(3,4,5)P₃ and PI(3,4)P₂. PI(3,4,5)P₃ is universally accepted as one of the most important second messengers in signal transduction. However, our knowledge of the functions of PI(3,4)P₂ as a lipi

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21

Boller, Danielle. "The role of PI3K signaling in neuroblastoma and glioblastoma /." Zürich, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253047.

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22

Sears, Daniel. "Identification of PI3K/Akt targets in chronic myeloid leukaemia." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505451.

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23

Hervieu, Vilches Alexia. "Understanding and targeting PI3K downstream of oncogenic Met mutant." Thesis, Queen Mary, University of London, 2015. http://qmro.qmul.ac.uk/xmlui/handle/123456789/33935.

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The Receptor Tyrosine Kinase (RTK) Met, overexpressed or mutated in cancer, plays a major role in cancer progression and represents an attractive target for cancer therapy. This study aimed to investigate whether PI3K plays a role in Met oncogenicity. Three cell models were used: (i) NIH3T3 cells expressing WT Met or the constitutively active mutant M1268T Met; (ii) U87MG glioblastoma cells, with endogenous WT Met constitutively activated due to an autocrine loop; (iii) A549 lung cancer cells expressing endogenous WT Met, activated upon binding exogenous HGF. Met dependent Rac1 translocation t

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24

Nunes, Tinoco Nunes. "Estudo funcional da via PI3K/AKT em Aedes aegypti." Botucatu, 2018. http://hdl.handle.net/11449/157112.

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Orientador: Jayme Augusto de Souza Neto<br>Resumo: Aedes aegypti é a espécie de mosquito emergente em áreas urbanas com maior impacto na saúde pública, sendo o principal vetor dos arbovírus dengue, Zika e chikungunya. Por esse motivo, se faz indispensável a compreensão de mecanismos moleculares associados a processos fisiológicos em A. aegypti, como resposta imune, comportamento e homeostase intestinal. Conforme observado em outros organismos, a via PI3K/AKT tem papéis importantes no metabolismo, na reprodução, na tolerância ao estresse e na imunidade. A quinase AKT atua como um regulador nega

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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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26

Torroba, Balmori Mª Blanca. "The Multiple Tasks Endured by PI3K during neural tube development." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/399595.

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Development of the spinal cord involves coordination between exposure to localized extracellular signals and controlled activation of intracellular signaling pathways. This way, neuroepithelial cells firstly proliferate apically to increase the progenitor pool and, later on, initiate neurogenic divisions giving rise to a variety of neuronal cell types. Class IA PI3Ks are heterodimeric enzymes (catalytic+regulatory subunits) activated by receptors tyrosine kinase (RTKs) or G protein coupled receptors (GPCRs) that, upon extracellular stimuli, modulate diverse target proteins through local produc

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27

Guerrero, Hernández Martina. "Targeting tumor microenvironment crosstalk through GPCR receptors and PI3K pathway." Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/667975.

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The tumor microenvironment (TME) is gaining momentum due to its contribution to cancer progression and therapy resistance. This TME has a direct crosstalk with tumor cells that involves the activation of different pathways. Follicular lymphoma (FL) is the most common indolent non-Hodgkin lymphoma. Although FL is generally characterized by slow progression and high response rates to therapy, it is still considered incurable, because almost virtually all the patients relapse. FL is probably the NHL with the highest dependence on microenvironment. PI3K is a common denominator transducing the sig

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Körtl, Thomas [Verfasser], and Sven A. [Akademischer Betreuer] Lang. "PI3K-Inhibition im Pankreaskarzinommodell / Thomas Körtl ; Betreuer: Sven A. Lang." Regensburg : Universitätsbibliothek Regensburg, 2019. http://d-nb.info/1199104353/34.

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Dobler, Melanie. "Analyse des PI3K-Signalwegs bei der Entstehung des duktalen Pankreaskarzinoms." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-172239.

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Cizkova, Magdalena. "Pronostic and Predictive Markers in Breast Cancer - PI3K Signaling Pathway." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T021.

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Les résultats des projets actuels apportent une information, sur différents aspects des rôles de la voie PI3K, dans le développement du cancer du sein, et la réponse au traitement. Les projets particuliers couvrent des sujets liés à la voie aux niveaux concernant les récepteurs de la famille HER, activant la voie PI3K, ainsi que PI3K et les effecteurs en découlant. Les effets pronostic et prédictif de la dérégulation de PI3K sont les sujets centraux de la recherche décrite ici. Une baisse d’expression de PI3KR1 est associée à une survie réduite dans notre cohorte de patients. Une attention par

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Stamatkin, Christopher W. "PHOSPHATIDYLINOSITOL 3-KINASE (PI3K) AS A THERAPEUTIC TARGET IN NSCLC." UKnowledge, 2014. http://uknowledge.uky.edu/pharmacy_etds/58.

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Deregulated activation of phosphatidylinositol 3-kinase (PI3K) pathway is central to many human malignancies. The functions of this pathway are critical for normal cell metabolism, proliferation, and survival. In lung cancers, the PI3K pathway activity is often aberrantly driven by multiple mutations, including EGFR, KRAS, and PIK3CA. Molecules targeting the PI3K pathway are intensely investigated as potential anti-cancer agents. Although inhibitors of the pathway are currently in clinical trials, rational and targeted use of these compounds, alone or in combination, requires an understanding

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32

Wang, Ling, and Shunbin Ning. "LMP1 Signaling Pathway Activates IRF4 through the PI3K-Src Axis." Digital Commons @ East Tennessee State University, 2017. https://dc.etsu.edu/etsu-works/6544.

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33

Tavelis, Christodoulos. "Investigating the potential role of PIP4Ks in PI3K/Akt signalling." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/investigating-the-potential-role-of-pip4ks-in-pi3kakt-signalling(e70d9473-5932-468a-bdad-01668a68db58).html.

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Class I phosphoinositide 3-kinases (PI3Ks) generate the essential lipid second messenger PtdIns(3,4,5)P3 which plays a key role in the regulation of numerous cellular processes including cell growth and survival, gene transcription, cytoskeletal organisation and glucose metabolism through its downstream effectors and in particular the serine/threonine protein kinase Akt. Therefore, the PI3K/Akt signalling plays a critical regulatory role in diverse cellular processes and its dysregulation is implicated in the pathogenesis of many human diseases including cancer and type 2 diabetes. Overexpress

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34

Fero, Daniel James. "The role of PI3K in Ephrin-A1 induced cell retraction." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3315045.

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Thesis (Ph. D.)--University of California, San Diego, 2008.<br>Title from first page of PDF file (viewed August 4, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 104-113).

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Mammana, Santa. "Evaluation of the PI3K/Akt/mTOR pathway in Multiple Sclerosis." Doctoral thesis, Università di Catania, 2017. http://hdl.handle.net/10761/3951.

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Background The PI3K/AKT/mTOR pathway is an intracellular signaling pathway that regulates cell activation. proliferation, metabolism and apoptosis. Increasing body of data suggests that alterations in the PI3K/AKT/mTOR pathway may result in an enhanced susceptibility to autoimmunity. Aim of our work was to evaluate the involvement of the mTOR pathway in the pathogenesis of autoimmune diseases, with particular focus on Multiple Sclerosis (MS). Multiple sclerosis (MS) is one of the most common chronic inflammatory diseases of the central nervous system leading to demyelination and neurodegenerat

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Balista, Priscila Alves. "Inibidores de fosfatidilinositol-3-cinase (PI3K) e neuroproteção mediada pela cascata de sinalização da Akt na fase aguda do modelo de Pilocarpina." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/17/17140/tde-17022011-144706/.

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Introdução: A epilepsia do lobo temporal (ELT) é a forma mais frequente de epilepsia em adultos. Um modelo experimental de ELT consiste na indução de status epilepticus (SE) em animais por administração de Pilocarpina. Este modelo induz mudanças patofisiológicas e comportamentais em ratos muito semelhantes às observadas em seres humanos com ELT. Apesar da literatura apresentar dados relacionados às respostas celulares, pouco se conhece a respeito do envolvimento de cascatas de sinalização com insultos epileptogênicos no sistema nervoso. A enzima fosfatidilinositol-3-cinase (PI3K) está envolvi

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Proctor, Victoria Kate. "Signalling pathways linking interleukin 13 receptor activation to lung epithelial cell function." Thesis, University of Bath, 2013. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589658.

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The passage of fluid, ions and macromolecules across the epithelium is controlled primarily by epithelial tight junctions. Altered epithelial permeability is associated with lung disease, and barrier function is impaired by the Th2 cytokine IL-13. This thesis investigates the signalling pathways involved in the modulation of the epithelial barrier by IL-13 stimulation. Initial experiments demonstrated that the human sub-bronchial epithelial cell line Calu-3 could be easily manipulated when grown using an air-liquid culture system. Expression of various key tight junction proteins was demonstra

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Levade, Marie. "Mécanismes moléculaires de la production et des fonctions plaquettaires : rôle de Vps34 et impact des inhibiteurs ciblés de kinases." Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30036.

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Les plaquettes sanguines jouent un rôle essentiel dans le maintien de l'intégrité des vaisseaux sanguins. En cas de brèche vasculaire, elles conduisent à la formation d'un clou hémostatique via des étapes successives d'adhésion, sécrétion et agrégation finement régulées et préviennent alors un saignement excessif. Les plaquettes jouent également un rôle critique dans les pathologies thrombotiques comme l'athérothrombose, ce qui en fait des cibles pharmacologiques majeures dans ces situations. Au cours de ma thèse, deux axes de recherche ont été abordés : (i) l'étude du rôle de la PI3-kinase de

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Galleiske, Hanne. "Experimentelle Evaluation der Bedeutung des PI3K/AKT-Signalweges für die Tumorstrahlenempfindlichkeit." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-227334.

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Hintergrund und Fragestellung/Hypothese Trotz verbesserter Diagnose und Therapiestrategien in der Behandlung von Plattenepithelkarzinomen des Kopf-Hals-Bereichs (HNSCC) in den letzten Jahrzehnten liegt das 5-Jahres-Überleben der Patienten bei nur etwa 60 %. Die hohe Mortalität ist zurückzuführen auf eine hohe Rezidivrate nach Radio- und Radiochemotherapie. Experimentelle und klinische Daten zeigen in dieser Tumorentität eine häufige Dysregulation des PI3K/AKT-Signalweges, der an verschiedenen Resistenzmechanismen beteiligt ist. Die Zielmoleküle des Signalweges sind involviert in DNA-Reparatur,

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Ferreira, Marília Gabriele Prado Albuquerque [UNESP]. "Expressão proteica da via PI3K/AKT/mTOR em mastocitomas cutâneos caninos." Universidade Estadual Paulista (UNESP), 2014. http://hdl.handle.net/11449/122032.

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Made available in DSpace on 2015-04-09T12:28:17Z (GMT). No. of bitstreams: 0 Previous issue date: 2014-02-28Bitstream added on 2015-04-09T12:47:46Z : No. of bitstreams: 1 000813877.pdf: 1968360 bytes, checksum: ba893fb51a41ad4d26fafd388f7a43d2 (MD5)<br>A via PI3K/AKT/mTOR está relacionada com a proliferação, síntese proteica, sobrevivência e motilidade das células. Mutações nesta via tem sido associadas com o processo carcinogênico de diferentes tipos tumorais. Atualmente, inibidores específicos de proteínas como a PI3K, AKT, mTOR, vem sendo testados com o intuito de otimizar a terapia antit

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McCarragher, Leeza Sarah Marie. "PI3K signalling blockade : a target for chemotherapeutic enhancement in breast cancer." Thesis, University of Sheffield, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401117.

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Walsh, Michael Hartley. "Phosphoproteomic investigation of differential signalling downstream of class IA PI3K isoforms." Thesis, Queen Mary, University of London, 2014. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8917.

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The PI3K family is central to numerous cellular processes in both health and disease. The class IA isoforms of PI3K control such outputs as proliferation, metabolism and survival through their well-characterised function as lipid kinases, with their signalling thought to predominantly mediated by the Akt/PKB protein kinase. However there exist other signalling routes, including from the lipid kinase activity through other effectors, but also through a protein kinase function of the class IA isoforms themselves. Mass spectrometry is a powerful tool which has been central to the recent advances

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Ferreira, Marília Gabriele Prado Albuquerque. "Expressão proteica da via PI3K/AKT/mTOR em mastocitomas cutâneos caninos /." Jaboticabal, 2014. http://hdl.handle.net/11449/122032.

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Orientador: Andrigo Barboza De Nardi<br>Coorientador: Mirela Tinucci Costa<br>Coorientador: Reneé Laufer Amorim<br>Banca: Rosemeri de Oliveira Vasconcelos<br>Banca: Daniel Guimarães Gerardi<br>Resumo: A via PI3K/AKT/mTOR está relacionada com a proliferação, síntese proteica, sobrevivência e motilidade das células. Mutações nesta via tem sido associadas com o processo carcinogênico de diferentes tipos tumorais. Atualmente, inibidores específicos de proteínas como a PI3K, AKT, mTOR, vem sendo testados com o intuito de otimizar a terapia antitumoral em seres humanos e animais. Além de potenciais

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Liao, Wenjing. "Targeting PI3K pathway to enhance cisplatin cytotoxicity in lung cancer models." Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/39671.

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Lung cancer is a leading cause of cancer deaths and is commonly diagnosed in both males and females. The cause of lung cancer is mainly attributable to cigarette smoking and aging, accounting for more than half of all lung cancer deaths. Non-small cell lung cancer (NSCLC) is the most common subtype of lung cancer (about 80%) compared to small cell lung cancer (SCLC) and it is normally subclassified into squamous cell carcinoma, adenocarcinoma and large cell carcinoma. Cisplatin-based treatments are the main first-line regimens for any stage of NSCLC, although platinum has over a 40-year histor

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Dong, Shuai. "Pharmacologic and Genetic Investigation of PI3K p110delta in Chronic Lymphocytic Leukemia." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1503066319794882.

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Brennan, Tracy A. "Abrogation of Cbl-PI3K Interaction Increases Bone Volume and Osteoblast Proliferation." Diss., Temple University Libraries, 2011. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/107475.

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Cell Biology<br>Ph.D.<br>Cbl is a multivalent protein that interacts with a number of signaling molecules that affect cell proliferation, migration and apoptosis. Although it is a downstream effector of growth factors, cytokines and integrin signaling all of which influence bone mass, very few studies have examined the role of Cbl in osteoblast proliferation and differentiation. To examine the role(s) of Cbl in the skeletal system we have focused specifically on phosphorylation of CblY737 since it is a unique to Cbl (not present on other family members) and upon phosphorylation by Src family k

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Butler, Dominika Ewelina. "Targeting of the PI3K/AKT/mTOR pathway in human prostate cancer." Thesis, University of York, 2014. http://etheses.whiterose.ac.uk/8531/.

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The tumour suppressor PTEN is frequently lost in advanced prostate cancer leading to over-activation of the PI3K/AKT/mTOR pathway. Therefore targeting of the PI3K signalling with pathway-specific inhibitors has been proposed as a therapeutic strategy. Inhibition of AKT and mTOR kinases in prostate cancer cell lines showed a decrease in cell viability and reduction in phospho-biomarkers expression. Although apoptosis was not induced, a decrease in cell migration and G1 cell growth arrest were observed in LNCaP cells. However, in primary prostate cultures activation of the Ras/MEK/ERK compensato

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Müller, Anja. "Multiple outcomes for PI3K/Akt/mTOR targeting in non-Hodgkin lymphoma." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2015. http://dx.doi.org/10.18452/17284.

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Wachstumsfaktor bedingte Aktivierung des PI3K/Akt/mTOR Signalweg wirkt positiv auf Vermehrung und Überleben. Konstitutive Aktivierung des Signalweges in NHL ist jedoch an Tumorprogression und Therapieresistenz beteiligt. Am Zelllinienmodell wurden zwei mögliche Therapiestrategien der PI3K/Akt/mTOR Inhibition erprobt, PI3K Inhibition mit BKM120 und horizontale Kombination von Zytostatika mit PI3K/Akt/mTOR Inhibitoren Erstens, BKM120 hat Antitumoraktivität in NHL und induziert Zelltod. Auf molekularer Ebene führt BKM120 vermittelte Dephosphorylierung von CDK1 an Y15 zur Aktivierung des M-Phase

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Ulbar, Francesca <1983&gt. "Studio della via di segnale PI3K/Akt/mTOR nelle Cellule Dendritiche." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5401/1/Ulbar_Francesca_tesi.pdf.

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Il trapianto allogenico di cellule staminali emopoietiche è spesso l’unica soluzione per la cura di diverse malattie ematologiche. La aGVHD è la complicanza più importante che si può avere a seguito del trapianto allogenico ed è causata dai linfociti T del donatore che riconoscono gli antigeni del ricevente presentati dalle APC. Eliminare o inattivare la APC del ricevente prima del trapianto potrebbe prevenire la aGVHD. Ad oggi non esistono farmaci specifici diretti contro le APC, sono però noti i meccanismi molecolari coinvolti nella sopravvivenza cellulare come la via di segnale di PI3K.

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Ulbar, Francesca <1983&gt. "Studio della via di segnale PI3K/Akt/mTOR nelle Cellule Dendritiche." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5401/.

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Il trapianto allogenico di cellule staminali emopoietiche è spesso l’unica soluzione per la cura di diverse malattie ematologiche. La aGVHD è la complicanza più importante che si può avere a seguito del trapianto allogenico ed è causata dai linfociti T del donatore che riconoscono gli antigeni del ricevente presentati dalle APC. Eliminare o inattivare la APC del ricevente prima del trapianto potrebbe prevenire la aGVHD. Ad oggi non esistono farmaci specifici diretti contro le APC, sono però noti i meccanismi molecolari coinvolti nella sopravvivenza cellulare come la via di segnale di PI3K.

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