Tesi sul tema "IKRK"
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Buehler, Christoph. "Gerechtigkeit am Kreuze Die Informationspolitik des IKRK aus ethischer Perspektive /". St. Gallen, 2006. http://www.biblio.unisg.ch/org/biblio/edoc.nsf/wwwDisplayIdentifier/02603496001/$FILE/02603496001.pdf.
Testo completoSchorr, Michael. "Der Wandel der humanitären Aktion internationaler Organisationen : die institutionellen sowie materiell-rechtlichen Konsequenzen dargestellt am Beispiel des IKRK, UNHCR und UNHCHR /". Hamburg : Kovač, 2004. http://www.gbv.de/dms/spk/sbb/recht/toc/373362889.pdf.
Testo completoEa, Chee-Kwee. "Ubiquitination-dependent activation of IKK". Access to abstract only; dissertation is embargoed until after 12/20/2006, 2005. http://www4.utsouthwestern.edu/library/ETD/etdDetails.cfm?etdID=125.
Testo completoDrew, Devin Lee. "Biophysical Characterization of NEMO and IKK₂". Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2006. http://wwwlib.umi.com/cr/ucsd/fullcit?p3239883.
Testo completoTitle from first page of PDF file (viewed January 12, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 110-121).
Criollo-Cespedes, Alfredo. "Regulation of autophagy by IP3R and IKK complex". Paris 11, 2009. http://www.theses.fr/2009PA11T099.
Testo completoHarris, Jennifer. "Regulation of nuclear factor kappa B subunit c-Rel through phosphorylation by two IKK-related kinases, IKK epsilon and TBK-1". Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=82250.
Testo completoMoreira, Bernardo Pereira. "Identificação dos microRNAs expressos em macrófagos estimulados com alta ou baixa dose de DNA plasmideal e avaliação dos seus papéis na cascata de sinalização". Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/17/17147/tde-05062012-142837/.
Testo completoOur group demonstrated that the capture of low doses of plasmid DNA can inhibit antigen presentation and induce an anti-inflammatory response pattern together with the decrease of pro-inflammatory cytokines expression, as observed in in vivo experimental models. Moreover, we observed that after the uptake of plasmid DNA by macrophages, these molecules could prevent endosomal vesicles acidification, an essential step for antigen presentation to CD4+ T cell. These results are in contrast with the usual DNA vaccines models commonly used. The low dose of plasmid DNA, in the context of immune response induction, can take to a modification in antigen presentation leading to the control of the response already established, what can be a potential treatment in auto-immune diseases and inflammation. The objective of this work is to identify expressed microRNAs on J774 macrophages triggered by different concentrations of plasmid DNA stimuli in order to evaluate the observed immunomodulatory mechanism. J774 macrophages were treated with low (10 µg/mL) and high (100 µg/mL) doses of pcDNA3 for 2 hours. Total RNA was extracted and microarray (Agilent plataform) was performed for detection of differentially expressed microRNAs. All obtained data was normalized in Genespring GX11.5 software. The microRNAs expression was confirmed by RT-qPCR and their mRNA targets were predicted by miRDB software. The miRNAs and their respective targets were also evaluated on DNA and LPS-treated macrophages. We detected 6 differentially expressed microRNAs (miR-494-3p, miR-21-3p, miR-1897-5p, miR-1894-3p, miR-294-3p e miR-483-5p) between the two conditions (fold change 2, p-value 0,05). The miR-494-3p expression increased only in cells treated with low dose of pcDNA3, on either previously LPS-stimulated cells or not. IBk (IKK-) was one of the predicted targets for miR-494-3p. RT-qPCR was performed to calculate its expression and its biological function was assessed by western blot. Besides, results from pcDNA3-treated cells from TLR9 knockout mice suggest that miR-494-3p expression is TLR9 independent although the receptor presence impaired miR-494-3p expression on high dose of pcDNA3-treated cells. Together, the data indicate that when macrophages are treated with low dose of plasmid DNA, miR-494-3p expression is increased, acting as negative regulator of the transcription factor NF-B, through IKK- inhibition.
Anderson, Jeff. "Genetic Analysis Of Specialized Tumor Associated Macrophages And Tumor Associated Fibroblast". The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1228083946.
Testo completoAljeffery, Abdullah. "The role of IKK alpha in prostate cancer bone metastasis". Thesis, University of Sheffield, 2019. http://etheses.whiterose.ac.uk/23005/.
Testo completoPerez, Jessica Marie. "Phosphorylation and mechanistic regulation of a novel IKK substrate, ITCH". Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1512569748748798.
Testo completoZhang, Jiazhen. "An investigation of the activation of protein kinase complexes in the MyD88 signalling network". Thesis, University of Dundee, 2017. https://discovery.dundee.ac.uk/en/studentTheses/de0ade75-5c10-4134-a7f7-27c2f315b58f.
Testo completoSimkovsky, Nadja Melitta. "Synthesis of some potential IKK inhibitors based around a pyrimidine scaffold". Thesis, University of Liverpool, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367619.
Testo completoAdli, Mezher Baldwin Albert Sidney. "Investigating the role of IKK epsilon in cancer-associated NF-kappaB activity". Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,1274.
Testo completoTitle from electronic title page (viewed Mar. 27, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Biology Graduate Studies in Molecular, Cell, and Developmental Biology." Discipline: Biology; Department/School: Biology. On t.p., Greek letters appear as symbols.
Asare, Yaw [Verfasser]. "Role of the COP9 signalosome and IKK complexes in Atherosclerosis / Yaw Asare". Aachen : Hochschulbibliothek der Rheinisch-Westfälischen Technischen Hochschule Aachen, 2013. http://d-nb.info/1044570229/34.
Testo completoWilson, Alastair. "Disrupting the inhibitory Kappa B kinase (IKK)-Aurora A axis in cancer". Thesis, University of Strathclyde, 2013. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=22402.
Testo completoForbes, Jonathan. "BIOCHEMICAL CHARACTERIZATION OF SUPPRESSOR OF IKK-ε AND NAK-ASSOCIATED PROTEIN 1". VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/86.
Testo completoBikman, Benjamin Thomas Dohm G. Lynis. "Modulation of IKK[beta] with AMPK improves insulin sensitivity in skeletal muscle". [Greenville, N.C.] : East Carolina University, 2008. http://hdl.handle.net/10342/1081.
Testo completoPresented to the faculty of the Department of Exercise and Sport Science. Advisor: G. Lynis Dohm. Title from PDF t.p. (viewed Apr. 23, 2010). Includes bibliographical references.
Sriskantharajah, Srividya. "The role of IKK-induced NF-κB1 p105 proteolysis in T lymphocytes". Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1446121/.
Testo completoRusilowicz, Emma Victoria. "Chemical biology approaches for the identification of novel p53 regulatory signalling pathways". Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/11774.
Testo completoBarken, Derren. "Temporal encoding and homeostatic control in the IKK-IkappaB-NF-kappaB signaling system". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3250073.
Testo completoTitle from first page of PDF file (viewed April 4, 2007). Available via ProQuest Digital Dissertations. Vita. Non-Latin script record Includes bibliographical references (p. 146-153).
He, Jiajia [Verfasser]. "Effects of IKK/NF-κB signaling in MYC-driven liver tumorigenesis / Jiajia He". Ulm : Universität Ulm, 2018. http://d-nb.info/1162953837/34.
Testo completoStellzig, Julia [Verfasser]. "The role of the non-canonical IKK complex in glioblastoma multiforme / Julia Stellzig". Gießen : Universitätsbibliothek, 2014. http://d-nb.info/106833052X/34.
Testo completoBaiget, Jessica. "Synthesis of inhibitors of the IKK-complex for the treatment of prostate cancer". Thesis, University of Strathclyde, 2012. http://digitool.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=25981.
Testo completoMcKinley, Sean W. "Using structural analysis to investigate the function of Suppressor of IKK-epsilon (SIKE)". VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3670.
Testo completoSabbaugh, Adam. "Characterizing the Effects of Mutant Huntingtin and IKK Beta on IL-34 Expression". Thesis, California State University, Los Angeles, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10270139.
Testo completoA major determinant of Huntington’s disease (HD) pathology is the expansion of a polyglutamine (polyQ) repeat in the exon-1 of Huntingtin protein (HTT). Proteolytic processing of mutant HTT liberates exon-1 (mHDx1) monomers, which oligomerize and disrupt cellular homeostasis. mHDx1 oligomers interact with various signaling proteins including the IkappaB kinase (IKK)/nuclear factor-kappaB (NF-κB) complex, a prominent regulator of inflammation. Neuroinflammation is implicated in the onset and progression of HD. A hallmark of neuroinflammation is the expansion of activated microglia in the central nervous system (CNS). Microglia communicate with neurons by several receptor-ligand systems. One is interleukin-34 (IL-34), a cytokine which plays a prominent role in microglial development and function. In the CNS, neurons produce and secrete IL-34, which binds to colony stimulating factor 1-receptor (CSF1-R) expressed by microglia. Factors that regulate neuroinflammation in Huntington’s disease remain unknown. For my thesis project, I participated in various experiments to determine whether mHDx1 influences IL-34 production in neurons. The accumulated data suggest that mHDx1 induces IL-34 expression in dopaminergic neurons derived from human embryonic stem cells. IL-34 production is also induced by stressful stimuli known to activate IKKβ. IKKβ-dependent aggregation of mHDx1 is critical for the production of IL-34. Secreted IL-34 has no visible effect on the aggregation of mHDx1 in neurons suggesting that it may influence other CNS cells such as microglia. Overall, my efforts helped to identify IL-34 production as a downstream effect of mHDx1 aggregation in neurons and will facilitate further studies on neuron-microglia communications in Huntington’s disease.
Hou, Yanjun. "Analysis Of The Ikkβ/Nf-Κb Signaling Pathway During Embryonic Angiogenesis And Tumorigenesis Of Breast Cancer". The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1222108300.
Testo completoLau, Rosanna. "cIAP2 Negatively Regulates Proliferation and Tumourigenesis by Repressing IKK Activity and Maintaining p53 Function". Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/22845.
Testo completoPaquette, Tyna. "Functional characterization of the E-4031 sensitive repolarization current, Ikr in rabbit ventricular myocytes". Thesis, McGill University, 1999. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=30722.
Testo completoSalem, Heba [Verfasser]. "Modulation of IKK/NF-kappaB signaling iin pancreatic β-cells induces diabetes / Heba Salem". Ulm : Universität Ulm. Fakultät für Naturwissenschaften, 2013. http://d-nb.info/1044350245/34.
Testo completoMittestainer, Francine Cappa 1986. "Ação anti-inflamatória da insulina = efeitos agudos sobre a via IKK/I'capa'B/NF-'capa'B". [s.n.], 2011. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311242.
Testo completoDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-19T22:12:54Z (GMT). No. of bitstreams: 1 Mittestainer_FrancineCappa_M.pdf: 2379142 bytes, checksum: cb6178fdb335fdabb4a29e4767a5c1b5 (MD5) Previous issue date: 2011
Resumo: A infusão da insulina durante a inflamação aguda melhora os resultados clínicos, mas o exato mecanismo desse efeito benéfico da insulina ainda não foi bem compreendido. Estudos recentes mostraram que a insulina tem um efeito antiinflamatório de modo que o hormônio também exibe um efeito inibidor sobre a mediação da transcrição de NF-kB em células mononucleares. Assim, o objetivo do presente estudo foi investigar os efeitos agudos da administração de insulina regular sobre a modulação de proteínas da via IKK/IkB/NF-kB e das proteínas chave da via de sinalização da insulina em tecido hepático, muscular e adiposo, a expressão de NF-kB nesses tecidos através de ELISA, o efeito do tratamento com insulina em macrófagos extraídos do peritônio de ratos e a influência dos inibidores da PI3K e MAPK na via inflamatória. Ademais, fizemos um ensaio da proteína fosfatase PP2A usando a imunoprecipitação com anticorpos anti-IKKbeta. Para o experimento, ratos machos adultos Wistar compuseram aleatoriamente 4 grupos diferentes. Três deles foram submetidos à infusão de insulina na veia porta e, então foram estimulados em 1, 3 e 5 minutos, enquanto o outro grupo (0) não foi estimulado com insulina. Em nossos resultados, observamos um aumento da fosforilação de IR, IRS1 e Akt induzida pela insulina nos três tecidos estudados. Em paralelo, houve uma redução na fosforilação de IKK e IkB após o estimulo da insulina. A ativação de NF-kB p65 no núcleo das células mostrou a redução na fosforilação do IKK e IkB no fígado, músculo e tecido adiposo. Na cultura de macrófagos tratada com insulina, após a adição dos inibidores específicos para PI3K e MAPK, observamos um aumento na fosforilação de IKK e IkB. Nossos resultados também mostraram que após estímulo da insulina houve um aumento na atividade da proteina fosfatase PP2A associada ao IKK nos três tecidos estudados. Desta forma, podemos sugerir que insulina pode induzir uma interação entre PP2A e IKK, o que resultará em mais desfosforilação de IKK e, assim, uma inibição da atividade da proteína quinase, revelando um potencial mecanismo de ação efeito anti-inflamatório da insulina
Abstract: Insulin infusion during acute inflammation improves clinical the outcomes but the exact mechanism of this beneficial effect is unclear. Recent studies have suggested that insulin has an anti-inflammatory effect in such a way that this hormone exhibits an inhibitory effect on the mediation of transcription of NF- kB in mononuclear cells. Thus, the aim of this study was to investigate the acute effects of regular insulin administration in modulation of IKK/IkB/NF-kB pathway and insulin signaling pathway (IR, IRS1 and Akt) and the DNA binding of NF-kB p65 in liver, muscle and adipose tissue of rats and also analyze the effect of treatment with insulin on macrophages of rats and the influence of PI3K and MAPK inhibitors on pathway. And finally, we analyze a phosphatase assay by using an immunoprecipitation with anti-IKKbeta antibody and PP2A phosphatase assay. For the experiment, male adult Wistar rats were divided in 4 groups. Three of them were submitted to insulin injection in the portal vein and were stimulated for 1, 3 and 5 minutes and the other group (0) was not stimulated (saline). In our results, we observed an increase in insulin-induced phosphorylation of IR, IRS1 and Akt during insulin injection in the three tissues studied. In parallel, there was a reduction in the phosphorylation of IKK and IkB after insulin stimulation. The DNA binding of NF-kB p65 in the cell nucleus showed a reduction of the IKK and IkB phosphorylation after insulin injection in liver, muscle and adipose tissue. In macrophages culture of treated with insulin and when added the specific inhibitor for PI3K and MAPK we observed an increased on phosphorylation of IKK and IkB. Our results also showed that after insulin stimulus there was an increase in PP2A phosphatase activity associated with IKK in the three tissues studied. Thus, we can suggest that insulin might induce an interaction between PP2A and IKK, which will result in more IKK dephosphorylation and thus an inhibition of this protein kinase activity, showed a possible anti-inflammatory effect of insulin
Mestrado
Mestre em Ciências
Niculaita, Roxana. "The role of AKT1 and IKK[beta] in ovarian cancer tumorigenesis and chemotherapeutic resistance". [Kent, Ohio] : Kent State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=kent1227665461.
Testo completoRastrick, Joseph. "The role of the IKK-2/NF-kB signaling in cigarette smoke-induced airway inflammation". Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/39413.
Testo completoLattke, Michael [Verfasser]. "Functional analysis of astroglial IKK/NF-KappaB signaling in brain development and homeostasis / Michael Lattke". Ulm : Universität Ulm. Fakultät für Naturwissenschaften, 2013. http://d-nb.info/1029507171/34.
Testo completoFong, Carol Ho Yan. "The anti-inflammatory role for IkappaB kinase (IKK) beta through inhibition of 'classical' macrophage activation". Thesis, Queen Mary, University of London, 2010. http://qmro.qmul.ac.uk/xmlui/handle/123456789/466.
Testo completoNeil, Jason Robert. "TGF-ß promotes cancer progression through the xIAP:TAB₁:TAK₁:IKK axis in mammary epithelial cells /". Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2008.
Cerca il testo completoTypescript. Includes bibliographical references (leaves 117-147). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;
Supekar, Vinit Mark. "Stress stimuli and pro-inflammatory kinases : structural studies of p38-α, -β2, -δ and IKK-α". Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619692.
Testo completoBaratchian, M. "Mechanism of IKK activation by the Kaposi's sarcoma-associated herpesvirus protein vFLIP and its cellular homologues". Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1461227/.
Testo completoKoppe, Christiane [Verfasser], Marc [Akademischer Betreuer] Spehr e Tom [Akademischer Betreuer] Lüdde. "Funktionen der IKK-Komplex-Untereinheiten in der Leberentzündung und Hepatokarzinogenese / Christiane Koppe ; Marc Spehr, Tom Lüdde". Aachen : Universitätsbibliothek der RWTH Aachen, 2016. http://d-nb.info/1126040940/34.
Testo completoIp, Wing Hang [Verfasser], e Thomas [Akademischer Betreuer] Dobner. "Modulation of cellular IKK complexes by human Adenovirus Type 5 / Wing Hang Ip ; Betreuer: Thomas Dobner". Hamburg : Staats- und Universitätsbibliothek Hamburg, 2017. http://d-nb.info/1134866089/34.
Testo completoKoppe, Christiane Verfasser], Marc [Akademischer Betreuer] [Spehr e Tom [Akademischer Betreuer] Lüdde. "Funktionen der IKK-Komplex-Untereinheiten in der Leberentzündung und Hepatokarzinogenese / Christiane Koppe ; Marc Spehr, Tom Lüdde". Aachen : Universitätsbibliothek der RWTH Aachen, 2016. http://d-nb.info/1126040940/34.
Testo completoCARTA, STEFANIA. "Role of the IKK/NF-κB pathway in the regulation of apoptosis during influenza virus infection". Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/202341.
Testo completoMikuda, Nadine. "The IkB kinase complex is a regulator of mRNA stability". Doctoral thesis, Humboldt-Universität zu Berlin, 2018. http://dx.doi.org/10.18452/19128.
Testo completoThe IKK complex is deemed to regulate gene expression through the activation of the transcription factor NF-kappaB. Here I describe an NF-kappaB-independent function of the IKK complex in regulating mRNA stability across different cell types and stimuli. A SILAC-MS screen for interaction partners of the regulatory subunit IKKgamma revealed an inducible interaction with Enhancer of mRNA Decapping 4 (EDC4). EDC4 is an essential component of cytoplasmic processing bodies (P-bodies). P-bodies function as sites of mRNA storage, degradation and miRNA-mediated silencing. Interaction between IKKgamma and EDC4 can be induced by various stimuli, including DNA damage, TNFalpha and IL-1beta. EDC4 was identified as a novel IKK substrate and four IKKbeta phosphorylation sites were determined by mass spectrometry and in kinase assays. Stable inducible cell lines, transient transfection and kinase inhibitors were used in different human cancer and in primary cell lines and demonstrated that phosphorylation of EDC4 by IKK is essential for formation of P-Bodies in response to numerous stimuli. mRNA stability assays confirmed stress-induced changes in the half-life of target mRNAs and revealed common regulation of mRNA stability by IKK and EDC4. The transcriptome-wide reach of this joint regulation was assessed via RNA-Seq analysis.
Rodrigues, Felipe Silva. "Explorando a quinase IKK como um alvo terapêutico para células iniciadoras de tumor pulmonares induzidas pelo oncogene KRAS". Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-26112018-080111/.
Testo completoThe most frequent genetic alterations in lung cancer are point mutations that activate the KRAS oncogene. Although these mutations are causally related to oncogenesis, different approaches to inhibit RAS proteins directly have not been successful to date. Therefore, for better therapeutic targets for lung cancer to become available, it is necessary to identify the molecular mechanisms activated by KRAS that are directly involved with important malignant features, such as the development and maintenance of a cancer stem-like phenotype by the tumour-initiating cells (TICs). TICs, also known as cancer stem cells, are defined as a subpopulation of tumour cells able to self-renew, promote tumour initiation, and sustain tumour growth. The development of therapeutic strategies to target these cells is imperative to improve the efficacy of antitumor therapy. Since KRAS is associated with the maintenance of a cancer stem-like phenotype and activates the transcription factor NF-kB through the IKKβ kinase to promote lung tumourigenesis, we hypothesised that IKKβ kinase contributes to the cancer stem-like phenotype induced by KRAS in lung cancer. We used tumoursphere formation assays to enrich and evaluate the function of TICs of KRAS-mutant cell lines A549 and H358. A549 and H358 cells formed tumourspheres in low adhesion culture and, when compared to cells grown in adherent culture, sphere-derived cells displayed increased clonogenic growth, higher expression of stemness genes by qPCR, and increased IKKβ kinase activity . Inhibition of IKKβ activity through a highly specific pharmacological inhibitor (Compound A) slightly decreased proliferation of A549 and H358 cells without inducing significant cell death. On the other hand, inhibition of IKKβ activity or expression by RNA interference reduced the expression of stemness genes and decreased tumoursphere formation. Inhibition of IKKβ expression in A549 cells also reduced TICs self-renewal . These results suggest that IKKβ plays an important role in maintaining the cancer stem-like phenotype of KRAS-driven lung TICs. Next, we demonstrated that IKKβ inhibition preferentially reduced cell proliferation and clonogenic growth of sphere-derived cells, suggesting that IKKβ plays a more important role in TICs than in adherent culture-derived cells. Flow cytometry analysis identified that sphere-derived cells display an enrichment for the surface marker CD24 in A549 cells and CD44 in H358 cells, indicating that these could be promising markers for the purification of TICs in these cell lines. Furthermore, we have shown by wound-healing assays of A549 and H358 cells that IKKβ inhibition reduced cell migration , another feature increased in TICs. In addition, we have shown that IKKβ activity in A549 and H358 cells does not depend on the MAPK or PI3K/Akt pathways. Interestingly, combined inhibition of IKKβ (a downstream effector of KRAS) and EGFR/ERBB2 (upstream regulators of KRAS that activate the MAPK and PI3K/Akt pathways) additively reduced tumoursphere formation, cell proliferation and migration. Taken together, our results suggest that IKKβ kinase plays an important role in the biology of KRAS-driven lung TICs, and that inhibition of this kinase alone or in combination with inhibition of other signalling pathways may represent a promising therapeutic strategy to be explored in order to reduce tumour recurrence and metastasis in KRAS-driven lung cancer.
Menagh, Gillian. "The regulation of Toll-like receptor (TLR)-stimulated inducible inhibitory kappa B kinase (IKK-i) expression in murine macrophages". Thesis, University of Strathclyde, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432751.
Testo completoNeto, Glauco Baiocchi. "Perfil da expressão imunoistoquímica de HER-2, NF-kB e IKK em câncer de colo uterino tratado com radioterapia". Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-24112011-154630/.
Testo completoINTRODUCTION: The standard treatment of early cervical cancer is radical hysterectomy and concomitant radiation therapy and chemotherapy for advanced stages. After radical hysterectomy, adjuvant radiation therapy is indicated if risk factors are present. HER-2 is part of protein membrane family that has a critical role in cellular differentiation, proliferation and survival. The NF-B regulates apoptosis, cellular cycle, adhesion and cellular migration. NF-B is activated by IKK kinase. NF-B activation is related to resistance to radiotherapy and chemotherapy. The overexpression of HER-2 may activate the NF-B pathway through PI3K/Akt. Our aims were: a) analyze the immunohistochemical expression of HER-2, NF-B-p50, NF-B-p65 and IKK in patients with cervical cancer treated with radiation therapy followed by radical hysterectomy; b) analyze the HER-2 amplification gene with FISH; c) evaluate the immunohistochemical expression of HER-2, NF-B-p50, NF- B-p65 and IKK as a prognostic factor to recurrence and death. MATERIALS AND METHODS: A retrospective analysis was carries out on 32 patients with cervical cancer submitted to radical hysterectomy after neoadjuvant radiotherapy from January 1992 to June 2001. RESULTS: The median age was 45 years (22-67). One patient was stage IB2 (FIGO) and 31 IIB (96,9%). All patients received external beam radiotherapy and high dose vaginal brachytherapy. Sixteen (50%) patients had residual pathological disease after radical hysterectomy. Median follow-up time was 73.5 months and overall 5-year survival was 66.5%. Immunohistochemical cytoplasmic expression of NF-B-p65 e NF-B-p50 before radiotherapy was found in respectively 90.6% and 96.9% of cases. Immunohistochemical nuclear expression of NF-B-p65 and NF-B-p50 before radiotherapy was found in both 59.4% of cases. Immunohistochemical cytoplasmic expression of NF-B-p65 and NF-B-p50 in the residual tumors after radiotherapy was found in both 50% of cases. Immunohistochemical nuclear expression of NF-B-p50 in the residual tumors was found in 75% of cases. There was no nuclear expression of NF-B-p65 in the residual tumors. Immunohistochemical expression of HER-2 was found in 21.9% of cases. However, gene amplification was found in one case (3.1%). There was no expression of IKK in neither primary nor residual tumors. HER-2 and NF-B were not correlated to the risk of residual tumor after radiotherapy. Immunohistochemical expression of HER-2 and NF-B were not correlated to risk of recurrence or death. CONCLUSIONS: Our data suggest that NF-kB is constitutively activated in advanced cervical cancer. NF-kB and HER-2 may not predict response to radiotherapy and do not correlate to poor outcome
Chen, Liang. "IkappaB Kinase beta in the Regulation of Cell Migration, Senescence and Fibrosis". University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1329495227.
Testo completoBenedetti, Giacomo. "Analisi computazionale e confronto con dati sperimentali della corrente rapida di potassio nei modelli di cardiomiocità ventricolare umano". Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2014. http://amslaurea.unibo.it/7093/.
Testo completoTomás, Hernández Sara. "Characterization of the biological effects of natural compounds against inflammation, metabolic syndrome and cancer". Doctoral thesis, Universitat Rovira i Virgili, 2017. http://hdl.handle.net/10803/456815.
Testo completoLos productos naturales han sido ampliamente utilizados para el tratamiento y prevención de muchas enfermedades. El objetivo principal de esta tesis es caracterizar compuestos naturales bioactivos que podrían utilizarse para la prevención o tratamiento de algunas enfermedades relevantes como son el síndrome metabólico, las enfermedades neurodegenerativas y el cáncer. Estas condiciones médicas representan un problema de salud importante ya que constituyen las principales causas de muerte a nivel mundial. Dado que numerosos estudios han demostrado que la inflamación crónica está directamente involucrada en la aparición del síndrome metabólico y las enfermedades neurodegenerativas, hemos intentado identificar compuestos naturales que puedan atenuar este persistente y nocivo estado de inflamación. Por ello, investigamos si el compuesto natural o-orsellinaldehido podría modular la respuesta inflamatoria actuando como inhibidor de IKK-2. Nuestros resultados confirman que el o-orsellinaldehido posee propiedades antiinflamatorias potentes sugiriendo que podría tratarse de un posible candidato preventivo o terapéutico para el tratamiento de patologías relacionadas con procesos de inflamación crónica como el síndrome metabólico y las enfermedades neurodegenerativas. Posteriormente, estudiamos los efectos antidiabéticos de otro compuesto natural, la 2,4,6-Trimethoxibenzofenona. Analizamos los efectos de este nuevo modulador selectivo de PPARγ en la inhibición de la fosforilación de la Ser273 de PPARγ mediada por la enzima CdK5, así como su influencia en la adipogénesis. Nuestros datos demuestran que la 2,4,6-trimetoxibenzofenona podría mejorar la resistencia a la insulina ya que es capaz de inhibir dicha fosforilación, y minimiza los efectos secundarios habituales de los fármacos existentes, como la adipogénesis, debido a la su baja actividad agonística. La última parte de la tesis tuvo como objetivo estudiar el efecto combinado de la quercetina y el resveratrol sobre el proceso autofágico en células HepG2, concluyendo que el resveratrol contrarresta potentemente la autofagia inducida por la quercetina bajo una situación de restricción calórica y sensibiliza las cáncerosas a la apoptosis.
Natural products (NPs) have been used for the treatment and prevention of many diseases and illnesses since early human history. The main goal of this doctoral thesis is the characterization of bioactive natural compounds that could be used for the prevention or treatment of some major significant diseases, such as metabolic syndrome, neurodegenerative diseases and cancer. These medical conditions constitute an important health problem worldwide since they are included in the world leading causes of death. Since numerous studies have shown that the chronic inflammation process is directly involved in the onset of metabolic syndrome and neurodegenerative diseases we aimed to identify NP that could mitigate this harmful persistent inflammation state. In that sense, we investigated if the natural compound o-oresllinaldehyde might modulate the inflammatory response by acting as IKK-2 inhibitor. Our results confirm that o-orsellinaldehyde possesses strong anti-inflammatory properties suggesting that it may be a potential preventive or therapeutic candidate for the treatment of pathologies that deal with chronic inflammation such as metabolic syndrome and neurodegenerative diseases. Then, we examined the anti-diabetic effects of another natural compound kwon as 2,4,6-Trimethoxybenzophenone. Concretely, we analyzed the effect of this novel selective PPARγ modulator (SPPARγM) on the Cdk5-mediated phosphorylation of PPARγ as well as its influence on adipogenesis. Our data demonstrated that 2,4,6-Trimethoxybenzophenone would retain the benefits of improving insulin resistance since its able to inhibit Cdk5-meditated PPARγ phosphorylation at ser273, but minimizes the common side effects of existent drugs, such as adipogenesis, by alleviating PPARγ agonistic activity. The last part of this thesis aimed to clarify the combined effect of the two natural compounds, Quercetin and Resveratrol, on the autophagic process in HepG2 cancer cells, concluding that resveratrol potently counteracts quercetin starvation-induced autophagy and sensitizes HepG2 cancer cells to apoptosis.
Vinolo, Emilie. "Etude structurale et fonctionnelle de mutations dans la protéine NEMO, régulateur essentiel de la voie de signalisation NF-kappaB, associées à des pathologies orphelines". Paris 6, 2006. http://www.theses.fr/2006PA066325.
Testo completoMaier, Eduard [Verfasser], Ralf C. [Gutachter] Bargou e Albrecht [Gutachter] Müller. "Molekulare Analyse des IKK-Komplexes als Zielstruktur für potentielle Therapieoptionen im Multiplen Myelom / Eduard Maier. Gutachter: Ralf C. Bargou ; Albrecht Müller". Würzburg : Universität Würzburg, 2016. http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127198.
Testo completo