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Dissertations / Theses on the topic 'IKRK'

Author: Grafiati

Published: 25 July 2024

Last updated: 31 July 2025

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1

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.

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2

Schorr, 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.

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3

Ea, 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.

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4

Drew, 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.

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Thesis (Ph. D.)--University of California, San Diego, 2007.<br>Title from first page of PDF file (viewed January 12, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 110-121).

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5

Criollo-Cespedes, Alfredo. "Regulation of autophagy by IP3R and IKK complex." Paris 11, 2009. http://www.theses.fr/2009PA11T099.

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6

Harris, 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.

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The nuclear factor kappaB (NF-kappaB) transcription factors are key regulators of immunomodulatory genes regulation. NF-kappaB activity is regulated through the phosphorylation of inhibitory proteins (IkappaBs) by the IkappaB kinase (IKK) complex (IKK alpha/beta/gamma), leading to IkappaB degradation and NF-kappaB translocation to the nucleus where they promote transcription of immunoregulatory genes. Moreover, cRel and p65 activities are also regulated by direct phosphorylation of their transactivation domain. Recently, two IKK non-canonical homologues, IKKepsilon and TBK-1 (TANK bindi

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7

Moreira, 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/.

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Nosso grupo demonstrou que a captura de baixas doses de DNA plasmideal pode inibir a apresentação de antígeno e induzir um padrão de resposta anti-inflamatória, e que após a captação do DNA plasmideal por macrófagos, estas moléculas podiam prevenir a acidificação de vesículas endossomais, um passo essencial para a apresentação de antígenos para células T CD4+. Além disso, em modelos in vivo, a baixa dose de DNA foi suficiente para amenizar o quadro inflamatório e diminuir a produção de citocinas inflamatórias. Estes resultados estão em contraste com os modelos de vacinas gênicas comumente util

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8

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.

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9

Aljeffery, Abdullah. "The role of IKK alpha in prostate cancer bone metastasis." Thesis, University of Sheffield, 2019. http://etheses.whiterose.ac.uk/23005/.

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IκB kinase subunit alpha (IKKalpha), a key component of the NFκB pathway, is implicated in prostate cancer progression and bone remodelling, but its role in the regulation of prostate cancer associated bone disease remains unknown. Here, we tested the effects of IKKalpha manipulation on prostate cancer cell behaviour in vitro and on osteolysis in a xenograft model of human prostate cancer bone metastasis. The pharmacological inhibition of IKKalpha using the novel and highly selective IKKalpha inhibitor SU1349 and stable knockdown of IKKalpha in PC3 cells significantly reduced cell viability, m

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10

Perez, 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.

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11

Zhang, 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.

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The TAK1 and canonical IKK complexes are the two master protein kinases of the innate immune system that control the production of inflammatory mediators, but the mechanisms by which they are activated in this system are still unclear. In this thesis, I present the research I have carried out to solve these problems. The IKKb component of the canonical IKK complex is required to activate the transcription factors NF-kB and IRF5 and the protein kinase Tpl2, but how IKKβ itself is activated in vivo is still unclear. It was found to require phosphorylation by one or more ‘upstream’ protein kinase

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12

Simkovsky, 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.

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13

Adli, 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.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2007.<br>Title 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.

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14

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.

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15

Wilson, 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.

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The IKK complex is an essential regulator of the NF-κB- signalling pathway. It is comprised of three sub-units; catalytic subunits IKKα and IKKβ and the catalytically inactive scaffolding protein IKKγ/NF-κB Essential Modulator (NEMO). The complex can be assembled in multiple conformations as either hetero- or homo-dimers of IKKα/β with or without the scaffolding protein IKKγ. This regulates NF-κB signalling and related cellular inflammatory responses that are often constitutively active in many cancer cells. Beyond regulation of NF-κB signalling a number of other potential IKK substrates have

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16

Forbes, Jonathan. "BIOCHEMICAL CHARACTERIZATION OF SUPPRESSOR OF IKK-ε AND NAK-ASSOCIATED PROTEIN 1". VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/86.

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Innate immunity provides the first line of defense against invading pathogen by recognizing and mounting a response to the pathogenic challenge. Among the cellular mechanisms of the innate immune response, Toll-like receptor 3 (TLR3) recognizes viral dsRNA and signals subsequent production of type-I interferon. The TLR3:interferon signaling cascades contains a kinase complex composed of two kinases and a scaffold protein, NAK-associated protein 1 (NAP1). The role of NAP1 in modulating kinase activation or regulation is unknown. A key inhibitory protein identified in the TLR3:interferon pathway

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17

Bikman, 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.

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Thesis (Ph.D.)--East Carolina University, 2008.<br>Presented 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.

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18

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/.

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Proteolysis of NF-kB1 p105 is vital for its function as a precursor to p50 and as an IkB. This occurs in two ways, both mediated by the proteasome. A constitutive proteolytic removal of the p105 C-terminus, termed processing, generates the mature transcription factor p50. In contrast, a signal-induced p105 proteolysis is triggered by phosphorylation of serines 927 and 932 in the p105 PEST region by the IKK complex. This promotes p105 poly-ubiquitination and subsequent complete degradation. IKK-induced p105 proteolysis has been demonstrated to regulate the kinase activity of the MAP3K TPL-2, si

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19

Rusilowicz, 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.

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p53 is a critical tumour suppressor which acts to repair or remove abnormal cells and thus prevent cancer. Aberrant function of p53 is therefore a critical step in tumourigenesis and p53 is mutated in half of all cancers. Mutation of p53 leads to both a loss of normal wildtype function as well as the gain of oncogenic function. p53 is considered to be a promising therapeutic target and therapeutic strategies for targeting of the p53 pathway include: 1. Activation of wild-type p53 (wtp53) protein function, 2. Refolding of mutant p53 (mtp53) into the wtp53 conformation, 3. Reduction of mtp53 pro

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20

Barken, 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.

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Thesis (Ph. D.)--University of California, San Diego, 2007.<br>Title 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).

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21

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.

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22

Stellzig, Julia [Verfasser]. "The role of the non-canonical IKK complex in glioblastoma multiforme / Julia Stellzig." Gießen : Universitätsbibliothek, 2014. http://d-nb.info/106833052X/34.

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23

Baiget, 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.

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Prostate cancer is the second most prevalent cancer in men. Activation of the NF-ҡB pathway is involved in the development of prostate cancer resistance to current therapies and contributes to the high mortality rate associated with this cancer. NF-ҡB has been shown to be inactive in the cytosol when bound with IҡB proteins. Activation of the IҡB kinase (IKK) complex degrades IҡB via phosphorylation and subsequent targeting by the proteasome, which enables transcription of NF-ҡB into the nucleus to control gene expression. The IKK-complex is formed by the two catalytic subunits IKKα and IKKβ a

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24

McKinley, 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.

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The innate immune system provides the body’s first line of defense against pathogenic challenge through pathogen recognition and initiation of the immune response. Among the various cellular mechanisms of pathogen recognition in mammals, Toll-like receptor 3 (TLR3) recognizes viral dsRNA. Stimulation of TLR3 signaling pathway leads to transcription of pro-inflammatory cytokines and type-1 Interferons. Suppressor of IKKε (SIKE) interacts with two kinases in the signaling pathway, IKKε and TANK binding kinase 1 (TBK1), inhibiting the transcription of type I interferons. Recently, the Bell Labora

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25

Sabbaugh, 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.

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<p> A 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 microgl

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26

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.

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27

Lau, 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.

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The cellular inhibitor of apoptosis protein (cIAP)-2 plays an important role in the protection against apoptosis by inhibiting the endogenous IAP inhibitor Smac, thus allowing other members of the IAP family, such as XIAP to block caspases. Additionally, cIAP2 functions as a ubiquitin ligase and mediates survival/proliferative signaling through NF-κB. cIAP2 is overexpressed in many human cancers and is believed to play an oncogenic role. This led to the development of small molecule IAP antagonists aimed at eliciting apoptosis in cancer cells. However, the loss of cIAP2 is also associated with

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28

Paquette, 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.

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The delayed rectifier potassium current IKr (hERG) participates in repolarization of the cardiac action potential and is implicated in one form of inherited Long QT Syndrome. The goal of this study was to characterize the biophysical properties of IKr in isolated rabbit ventricular myocytes and hERG expressed in a mammalian cell line using mathematical, electrophysiological and molecular biological techniques. Incorporation of results into a mathematical gating model of IKr revealed that the current did not follow the typical Hodgkin-Huxley type gating formulation and therefore comprised a gat

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29

Salem, 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.

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30

Mittestainer, 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.

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Orientador: Mário José Abdalla Saad<br>Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas<br>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<br>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

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31

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.

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32

Rastrick, 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.

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Chronic Obstructive Pulmonary Disease (COPD) is an inflammatory lung disease largely associated with cigarette smoke (CS) exposure. The mechanism by which CS leads to the pathogenesis of COPD remains unclear, however many inflammatory mediators present in the COPD lung are thought to be regulated by the transcription factor Nuclear Factor-kappaB (NF-kB) and its upstream signalling kinase, Inhibitor of kB kinase-2 (IKK-2). The IKK- 2/NF-kB signalling pathway may therefore be crucial in the pathogenesis of the inflammation associated with COPD. To investigate this hypothesis, mice were exposed t

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33

Lattke, 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.

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34

Fong, 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.

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Recent research has revealed a role of NF-B in the resolution of inflammation. Using Cre-lox mediated gene targeting, IKK was selectively deleted in macrophages (IKKβ∆Mye). From in vitro studies, LPS stimulated IKKMye macrophages increased STAT1 phosphorylation, iNOS, MHC II and IL-12 production, suggesting negative cross talk between NF-B and STAT1 signalling pathways. Since IKK is required for TNF gene expression and TNF signalling, I investigated the hypothesis that TNF inhibits ‘classical’ macrophage activation through IKK activation. Macrophages from p55-/- and mice treated with

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35

Neil, 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.

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Thesis (Ph.D. in Pharmacology) -- University of Colorado Denver, 2008.<br>Typescript. Includes bibliographical references (leaves 117-147). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;

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36

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.

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37

Baratchian, 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/.

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Activation of the NF-κB pathway is linked to cancer development and progression. Kaposi’s sarcoma-associated herpesvirus (KSHV/HHV8) encodes vFLIP which binds to the NEMO/IKKγ subunit of IKK and constitutively activates NF-κB, leading to tumourigenesis. Cellular FLIPs, which share sequence homology with KSHV vFLIP and induce NF-κB activation, are upregulated in a variety of malignancies and are therefore promising targets for anti-cancer therapies. The cFLIP family consists of three splice variant isoforms (cFLIPL, cFLIPS and cFLIPR) and two proteolytic fragments (p43-FLIP and p22-FLIP). Much

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38

Koppe, Christiane [Verfasser], Marc [Akademischer Betreuer] Spehr, and 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.

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39

Ip, Wing Hang [Verfasser], and 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.

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Koppe, Christiane Verfasser], Marc [Akademischer Betreuer] [Spehr, and 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.

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CARTA, 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.

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The influenza virus represents one of the most important viral pathogens causing respiratory illness in humans and in animals. New influenza virus strains are constantly produced by protein mutation (antigenic drift) or genome reassortment (antigenic shift) and this high variability determines a resistance to antiviral drugs. In the recent years, the emergence of new avian and swine influenza A virus strains able to infect humans represents a serious threat to global human health. Given the high mutation rate of the viral proteins, a more innovative approach to anti-influenza therapy is the se

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Mikuda, 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.

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Bisher wurde davon ausgegangen, dass der IKK-komplex durch Regulation des Transkriptionsfaktors NF-kappaB die stressinduzierte Expression von Zielgenen steuert. Im Rahmen der hier vorgelegten Dissertation konnte jedoch gezeigt werden, dass der IKK-Komplex unabhängig von seiner Rolle in der NF-kappaB-Aktivierung die Stabilität einer Vielzahl von mRNAs kontrolliert. Mittels der Kombination von Ko-Immunopräzipitationsstudien und SILAC-MS konnte die induzierte Interaktion der regulatorischen Untereinheit des IKK-Komplexes IKKgamma mit dem Gerüstprotein EDC4 (Enhancer of Decapping 4) nachgewiesen w

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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/.

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As alterações genéticas mais frequentes em câncer de pulmão são mutações pontuais que ativam o oncogene KRAS. Embora estas mutações estejam causalmente relacionadas à oncogênese, até hoje diferentes abordagens para inibir as proteínas RAS diretamente não obtiveram sucesso. Portanto, para que melhores alvos terapêuticos para o câncer de pulmão se tornem disponíveis é necessário identificar os mecanismos moleculares ativados por KRAS que estão diretamente envolvidos com a aquisição de propriedades malignas importantes, como o desenvolvimento e a manutenção de um fenótipo tronco-tumoral pelas cél

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44

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.

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45

Neto, 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/.

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INTRODUÇÃO: O tratamento padrão do câncer do colo uterino é a histerectomia radical para doença inicial e quimio-radioterapia para doença avançada. A radioterapia após a histerectomia radical tem impacto em ganho de sobrevida caso hajam fatores de risco histopatológicos para recidiva. Portanto, a busca de marcadores preditores de radiossensibilidade torna-se importante para a individualização do planejamento terapêutico. O HER-2/ErbB-2 faz parte da família de proteínas ErbB que formam um grupo de receptores de membrana e tem um papel crítico no controle de diversas funções celulares básicas co

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46

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.

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Benedetti, 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/.

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Tomás, 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.

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Abstract:

Els productes naturals han sigut àmpliament utilitzats per al tractament i prevenció de moltes malalties. L’objectiu principal d’aquesta tesi ha estat caracteritzar compostos naturals bioactius que podrien ser utilitzats per a la prevenció o tractament d’algunes malalties rellevants com ara la síndrome metabòlica, les malalties neurodegeneratives i el càncer. Aquestes condicions mèdiques representen un problema de salut important ja constitueixen les principals causes de mort a nivell mundial. Atès que nombrosos estudis han demostrat que el procés d’inflamació crònica està directament involu

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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.

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Maier, Eduard [Verfasser], Ralf C. [Gutachter] Bargou, and 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.

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