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Debiparshad, Kevin. "Musculoskeletal phenotype of Egr-1 deficient mice." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86749.
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Early growth response protein-1 (EGR-1) is a transcription factor induced by stress or injury, mitogens, and differentiation factors. It has been shown to be regulated by various cytokines, growth factors and by ischemic/hypoxic stress as well as shear stress and mechanical injury. These regulators have been linked to both the development as well the degeneration of the musculoskeletal system, namely articlar cartilage, intervertebral discs (IVDs) and bone. Furthermore, Egr-1 has been shown to regulate the expression of collagens and enzymes affecting the extracellular matrix. Polymorphisms of DNA binding sites for EGR-1 have shown to be associated with both disc degeneration and osteoporosis. The aim of this study was to determine the affects of EGR-1 deficiency on articular cartilage, IVD and bone phenotype.Wild-type (+/+) C57Bl/6 or Egr-1-deficient (−/−) mice were sacrificed at the same age interval (8- to 9-months). Standard histological preparation and staining with Safranin-O/Fast Green were done. Also immuncohistochemistry was performed using anti-bodies to type X collagen, cleavage products of both type II collagen and aggrecan. Imaging of mice was with plain radiographs, bone mineral density measurements and microCT analysis.
Results revealed that these mice have differences including abnormal bone structure and density, structural and possibly compositional differences in articular cartilage and structural and biochemical changes in IVDs. This points to the importance of Egr-1 in the maintenance of normal bone, IVD and articular cartilage and makes it a possible target for initiating pathological conditions of these tissues.
La protéine de croissance EGR-1 (Early Growth Response protein-1, en anglais) est un facteur de transcription qui est induit par la tension ou la blessure, les facteurs mitogènes, et les facteurs de différenciation. EGR-1 est ainsi régulé par divers cytokines, facteurs de croissance, par les conditions ischémique, ainsi que la tension et les blessures mécaniques. Ces régulateurs ont été reliés au développement ainsi que la dégradation du système squeletto-musculaire, particulièrement le cartilage articulaire, les disques intervertébraux (DIV) et l'os. De plus, il a été démontré que EGR-1 peut réguler l'expression des collagènes et d'enzymes contribuant à la matrice extracellulaire. Le polymorphisme de séquences d'ADN pour les des sites d'attachements d'EGR-1 a démontré être associé avec la dégradation de disques intervertébraux et l'ostéoporose. L'objectif de cette étude était de déterminer l'effet d'une expression réduite d'EGR-1 sur les phénotypes du cartilage articulaire, les DIV, et l'os.
Les souris C57Bl/6 de phénotype sauvage (+/+) ou ceux avec une expression réduite d'EGR-1 (−/−) ont été sacrifiées au même intervalle d'âge (8 à 9 mois). La préparation histologique standard et la coloration avec Safranin-O/Fast Green a été fait. Aussi l'immunohistochimie a été exécuté avec des anticorps pour le collagène de type X, et les produits de clivage du collagène de type II ainsi que les aggrécanes. L'imagerie de souris a été faite avec les radiographies simples, les mesures de densité minéraux de l'os, et avec l'analyse de micro-tomodensitomètre.
Les résultats ont révélé que ces souris ont des différences incluant la structure et densité d'os anormaux, les différences structurelles et possiblement compositionnelles dans le cartilage articulaire, et les changements structurels et biochimiques dans les DIV. Ceci indique à l'importance d'EGR-1 dans l'entretien d'os normal, des DIV et le cartilage articulaire, et le rend une cible possible pour initier les conditions pathologiques de ces tissus.
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Owen, Jo. "Structural and functional studies of fibulin-1 EGF domains." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270656.
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Maifrede, Silvia. "EGR-1 TUMOR SUPPRESSOR IN BCR-ABL DRIVEN LEUKEMIA." Diss., Temple University Libraries, 2015. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/321048.
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Molecular Biology and GeneticsPh.D.
Chronic Myelogenous Leukemia (CML) is a hematological disease originated with a chromosomal translocation t(9;22)(q34;q11) in a pluripotent hematopoietic stem cell. CML typically evolves in 3 different clinical phases: chronic and accelerated phases, and blast crisis. Disease progression is associated with the acquisition of secondary mutations that can be of very diverse origins, including inactivation of tumor suppressor genes, as well as inhibition of differentiation, DNA repair and telomere maintenance. While current therapies are very often successful, the remaining issues of resistance and the fact that therapy will not cure CML make it important that new therapy capable of effectively curing it be developed. The early growth response-1 (Egr-1) gene is a zinc-finger transcription factor localized to the human chromosome 5. Egr-1 belongs to a family of early response genes whose expression is rapidly stimulated by growth factors, hormones and neurotransmitters. In addition, Egr-1 is a myeloid differentiation primary response (MYD) gene, and is a positive regulator of terminal myeloid differentiation that potentiates macrophage differentiation. It also has been shown that Egr-1 plays a role in the development, growth control and survival of several cell types, such as T cells, B cells, and neuronal cells in addition to myeloid cells. There is a large amount of evidence consistent with Egr-1 behaving as a tumor suppressor in hematopoietic cells, both in vivo & in vitro, in both humans & mice, making it a prime candidate for a role in CML. In this study we asked if Egr-1 would behave as a tumor suppressor in CML. To answer that we investigated the function of Egr-1 in BCR-ABL driven leukemia using a mouse m bone marrow transplantation (BMT) model. We observe that loss of Egr-1 accelerates the onset of BCR-ABL driven CML. Furthermore, through Facs analysis we showed that most animals developed myeloid leukemia, determined by the observation that the majority of GFP+ cells in the BM were positive for Gr-1 and negative for B220. Interestingly a small cohort of mice developed B-cell acute lymphoid leukemia (B-ALL); this included both WT BCR-ABL and Egr-1 KO BCR-ABL BM-transplanted groups. In addition, we demonstrated that the loss of Egr-1 caused a more aggressive leukemia, which resulted not only in more rapid onset of disease but also greater enlargement of spleen and liver, as well as a tendency to more aggressive lung infiltration of leukemic cells. We also showed that decreased apoptosis, increased proliferation rates and resulting increased viability are consistent with, and probably contribute to, the increased leukemic potential of Egr-1 KO BCR-ABL BM. In addition, we demonstrated that Egr-1 expression was downregulated in BCR-ABL expressing BM cells in vitro, and in spleens of transplanted leukemic mice. Moreover, a very interesting observation, consistent with the rapid onset and aggression of disease, was that the bone marrow of leukemic mice caused by Egr-1 KO BCR-ABL BM transplantation, were enriched with lineage negative BCR-ABL-expressing cells, significantly more so than what was observed in WT BCR-ABL-transplanted mice. That this is also an enrichment of leukemia initiating cells was demonstrated using bone marrow from primary transplantation in a secondary bone marrow transplantation assay. Furthermore, using serial replating assays of colony forming units (CFUs), it was demonstrated that Egr-1 KO BCR-ABL-expressing BM had higher self-renewal ability than WT BCR-ABL-expressing BM, exhibiting an enrichment of primitive stem cells and fewer differentiated cells relative to WT counterparts. Finally, we also analyzed expression of Egr-1 in samples of CML human patients; the results are intriguing but due to small sample size inconclusive. Further inquiry on Egr-1 in CML, including expanding the study of human CML, signaling analysis, interaction of Egr gene family members in leukemia, and gain of function experiments should identify novel players that can impact on the aggressiveness of the disease, predict outcome for currently established therapies, as well identify targets for treatment regimens or adjunct therapy. In addition, these studies can provide a paradigm for understanding how Egr-1 functions as a tumor suppressor for other cancers and types of leukemia, and also delineate pathways that can be activated/inhibited by drugs, including reactivating Egr-1 expression.
Temple University--Theses
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Hashim, Irshaad. "The Effect of Freud-1/CC2D1A Knockout on EGF Receptor Activation." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/33400.
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CC2D1A (coiled-coil and C2 domain containing protein 1A), also known as Freud-1, has been identified as a transcriptional repressor of the serotonin receptor 5-HT1A, a regulator of endosomal budding and an activator of NF-KB signaling. It also acts as a scaffold that promotes activity of the PI3K/Akt pathway upon stimulation by the epidermal growth factor (EGF). Moreover, several studies highlight naturally occurring mutations of CC2D1A in humans that produce varying degrees of intellectual disorder and autism.
Use of the Cre-LoxP system to conditionally knockout CC2D1A in mice has provided promising results regarding its effect on 5-HT1A expression and behaviour. This thesis aims to extend the use of this knockout model by studying cell signaling activity in mouse embryonic fibroblasts (MEFs), derived from the CC2D1Aflx/flx transgenic line, that have been treated with a commercially available Cre recombinase to completely knock out CC2D1A. I hypothesize that CC2D1A directly regulates EGF receptor activity and that its Cre-mediated knock down in vitro will entirely block cell signaling pathways activated by the EGF receptor.
Western blot analysis demonstrated that, after Cre-mediated CC2D1A knockout, Akt and Erk1/2 phosphorylation were still maintained upon EGF treatment. In addition, overexpressing Freud-1 via transfection had no effect on cell signaling compared to the wild-type control. Analysis of recombinant Freud-1 constructs reveal that a C-terminal truncation enhances its ability to bind to PIP2 and PIP3 – phospholipids essential to the Akt pathway. In addition, immunocytochemistry analysis demonstrates a responsiveness of CC2D1A to EGF treatment. Altogether, these data highlight a unique and effective way in carrying out gene knockout in vitro while also emphasizing the need to further investigate CC2D1A’s importance in regulating cell signaling pathways and functional compensation by other homologous proteins
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Gallagher, Ewen. "The regulation of the egr-1 promoter in B cell lines." Thesis, University of Nottingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341970.
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Lee, Jeffrey Robson. "Mechanism of Drosophila EGF receptor activation by Rhomboid-1 and Star." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619660.
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Kasneci, Amanda. "Early growth factor response 1 (Egr-1) negatively regulates expression of calsequestrin (CSQ) on cardiomyocytes in vitro." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112521.
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Heart failure represents an important cause of death in Western Countries. The pathophysiology of heart failure is mainly associated with abnormalities in intracellular calcium control. We previously showed that Egr-1 negatively regulates expression of sodium-calcium exchanger (NCX) in vivo and in vitro. Here we tested the hypothesis that Egr-1 regulates expression of calcium storage proteins in the sarco-endoplasmic reticulum (SER), calsequestrin (CSQ) and/or ER, calreticulin (CRT) directly or indirectly via Egr-1:NFAT (nuclear factor of activated T-cells) formation. Secondarily, we hypothesized that this will reduce calcium mobilization. We found that undifferentiated 1293F cells, overexpressing Egr-1, have reduced CSQ compared to control H9c2 cells. We demonstrated that Egr-1 negatively regulates CSQ but not CRT expression. The Egr-1 mediated decrease in CSQ is linked to decreased calcium availability. Repression is by a novel NAB-independent (NGFI-A binding protein) activity localized to a.a. region 1-307. We conclude that Egr-1-mediated reductions in calcium storage protein expression alter calcium availability for cardiac contraction/relaxation.
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Shao, Zhiyong. "Roles of Caenorhabditis elegans EGL-9 in HIF-1 regulation and pathogen resistance." [Ames, Iowa : Iowa State University], 2010. 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:3403833.
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Messai, Habib. "Insulin-like growth factor I (IGF-I), Epidermal growth factor (EGF), Endothéline-1 (ET-1) et vieillissement des chrondrocytes articulaires." Paris 7, 2001. http://www.theses.fr/2001PA077101.
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LIMA, Jacqueline de Souza. "Diversidade Genética e estrutura espacial intrapopulacional em Tibouchina papyrus(POHL) Toledo utilizando marcadores microssatélites." Universidade Federal de Goiás, 2011. http://repositorio.bc.ufg.br/tede/handle/tde/2555.
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Previous issue date: 2011-02-25Tibouchina papyrus is a Melastomataceae endemic to the Cerrado. It has a disjunct distribution, restricted to campos rupestres . Therefore, it can be considered a model species, helping guide Cerrado endemic plant studies. Thus, this study aimed to characterize genetic variability in microsatellite regions of T. papyrus genome and use spatial statistical analysis methods to assess genetic diversity and structure in disjunct populations. Individuals were georeferenced and leaf samples were taken from the localities of Serra dos Pirineus (216), Serra Dourada (66) and Serra de Natividade (192). In order to obtain the genotypes, we used ten microsatellite loci that were developed for T. papyrus. The locus showed a mean of 3,4 alleles and a large number of private alleles was detected (19 in total) at the populations studied. Values (f) significant were observed for two populations, indicating that populations not are following the proportions expected by Hardy-Weinberg. The global value is significant and equal to 0.712, showing a high differentiation among the three populations studied. Thus, the three populations of T. papyrus can be treated as three different ESUs. Spatial genetic structure was weak for two populations, with low levels of SP. The low SGS corroborates the hypothesis that wind-dispersed species present no SGS due to long distance gene flow because of seed dispersal. This is plausible for T. papyrus, which is a wind-dispersed species. Despite the low intra-population SGS found in two populations, based on the relationship between kinship and distance, significant positive values were observed for the some distance class, indicating higher values for the relationship between these individuals. The intercept of the correlogram for each population may indicate the minimum distance where it is more likely that sampled individuals are less similar, which is an information applicable for the management of T. papyrus populations. Based on genetic data, it was evident that the three T. papyrus populations must be preserved, because each one contains a number of unique genetic variability that is not shared between them. Thus, theoretically it is possible to maintain the evolutionary potential of this species and to avoid local extinction in only three regions where it occurs.
Tibouchina papyrus é uma Melastomataceae endêmica do Cerrado que possui distribuição disjunta e restrita aos campos rupestres, com essas características peculiares ela pode ser considerada modelo de espécie, auxiliando em estudos de outras plantas do Cerrado que exibem o mesmo conjunto de características. Neste sentido, o objetivo desse trabalho foi caracterizar a variabilidade genética existente em regiões microssatélites do genoma de T. papyrus e utilizar metodologias de análise estatística espacial para avaliar a diversidade e a estrutura genética nas três subpopulações disjuntas da espécie. Foram amostradas folhas e georreferenciados indivíduos nas Serras dos Pirineus (216) Serra Dourada (66) e Serra de Natividade (192). Para a obtenção dos genótipos foram utilizados dez locos microssatélites desenvolvidos para a espécie. Os dez locos produziram uma média de 3,4 alelos e foi detectado um grande número de alelos privados (19 no total) nas três subpopulações avaliadas. Foi observados valores de (f) significativos em duas subpopulações, indicando que estas subpopulações não estão seguindo as proporções esperadas para o equilíbrio de Hardy-Weinberg. O valor global de θ foi significativo e igual a 0,712, apresentando uma altíssima divergência genética entre as subpopulações. Sendo assim, as três subpopulações de T. papyrus podem ser tratadas como três diferentes ESUs. A estrutura genética espacial intrapopulacional apresentou-se fraca em duas subpopulações, com baixos níveis de SP. A existência de autocorrelação espacial pouco intensa corrobora com a hipótese de que espécies com dispersão pelo vento não exiba esta estrutura, em função do fluxo gênico causado pela dispersão de sementes em longas distâncias. Isso é plausível para T. papyrus, que apresenta dispersão por anemocoria. Apesar da fraca EGE intrapopulacional encontrada em duas subpopulações, baseado nos correlogramas de parentesco, foram observados valores positivos e significativos nas primeiras classes de distância, indicando um maior grau de parentesco entre esses indivíduos. O intercepto do correlograma para cada uma das subpopulações pode indicar o distanciamento mínimo onde é mais provável amostrar indivíduos menos semelhantes, que é uma informação relevante para o manejo das subpopulações da espécie T. papyrus. Com base nos dados genéticos obtidos ficou evidente que as três subpopulações da espécie T. papyrus devem ser conservadas, pois cada uma contém uma quantidade de variabilidade genética única que não é compartilhada entre elas. Sendo assim, teoricamente torna-se possível a manutenção do potencial evolutivo da espécie e evita a extinção local nas três únicas regiões de ocorrência natural da espécie.
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Maroski, Bastian [Verfasser]. "Zeitliche Expression des Transkriptionsfaktors EGR-1 und der MAP-Kinasen ERK-1/2 in murinen Modellen der viralen Myokarditis / Bastian Maroski." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2016. http://d-nb.info/1113011726/34.
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Molle, Alexander. "Zur Beurteilung "begleitender" Wettbewerbsverbote im Rahmen von Art. 81 Abs. 1 EG und [section] 1 GWB." Heidelberg Müller, 2005. http://deposit.ddb.de/cgi-bin/dokserv?id=2633831&prov=M&dokv̲ar=1&doke̲xt=htm.
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Pasetto, Silvana. "Distribuição do EGF, EGFr, TGF-'beta'1, IL-1'alfa' e CSF-1 no periodonto de incisivos inferiores de ratos, em condições funcionais normal e alterada : estudo imunohistoquimico." [s.n.], 2005. http://repositorio.unicamp.br/jspui/handle/REPOSIP/288491.
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Orientador: Pedro Duarte NovaesTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
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Resumo: O objetivo deste estudo, foi analisar, por meio da técnica de imunohistoquímica, a distribuição do EGF, EGFr, TGF-b1, IL-1a e CSF-1, em 3 diferentes regiões dos incisivos inferiores de ratos, em condições funcionais normais e alteradas. Cinquenta animais, tiveram seus incisivos inferiores esquerdos, seccionados na altura da papila interdental, permanecendo fora de oclusão, sendo considerados hipofuncionais (Ho), seus contralaterais, em sobrecarga de função foram chamados hiperfuncionais (Hr). Vinte e cinco destes animais, sofreram a intervenção apenas uma única vez, sendo sacrificados 8 horas após, os outros vinte e cinco animais, sofreram a intervenção a cada 2 dias, sendo sacrificados no 8o dia de desoclusão. Dez animais pertencentes ao grupo controle (c), tiveram seus incisivos mantidos em condições funcionais normais de erupção. As hemimandíbulas de todos os animais foram fixadas em Karnovsky (com 0,1% de glutaraldeído), descalcificadas em EDTA 4,13%, subdivididas transversalmente em 5 regiões e incluídas em paraplast. Cortes transversais, com 4 mm de espessura de cada peça foram coletados em lâminas silanizadas e submetidos à técnica de imunohistoquímica. O folículo dental e o ligamento periodontal, mostraram variações nas intensidades de marcação, com todos os anticorpos, entre as diferentes regiões e entre os grupos analisados. Aparentemente, no entanto, os tecidos periodontais dos incisivos, após 8 dias de hipofunção, mostraram imunoreatividade mais forte, particularmente com o CSF-1, quando comparados com os incisivos, em condições funcionais normal e alterada. Os resultados parecem sugerir, que a ¿cascata¿ formada por essas moléculas, pode estar relacionada com a ampliação da via eruptiva do incisivo, que cresce por um período prolongado da vida do animal
Abstract: The aim of this study, was to analized, using immunohistochemical technique, the distribution of EGF, EGFr, TGF-b1, IL-1a e CSF-1, in periodontal tissues of three regions of rat lower incisors, in normal and altered functional conditions. Fifty animals, had their left lower incisors, cut at the level of the interdental papilla. Becoming out occlusion, they are considered hipofunctional teeth. The contralateral incisors, attrited with both upper incisors are considered hiperfunctional teeth. Twenty-five of these animals were killed 8 hours after. In the order twenty-five animals, the shortening was repeated every second day, and killed 8 days after. Ten animals were kept in normal functional conditions. The hemimandibules of all animals were fixed in Karnovsky (with 0,1% of glutaraldehyde), demineralized with EDTA, subdivided in five transversal regions and embedded in paraplast. Cross sections, 4 mm-thick were collected in glass slides coated with silane. The antibodies were developed with DAB plus H2O2. The dental follicle and the periodontal ligament showed variation in the staining intensities, for all antibodies used, among the different regions and groups analyzed. Apparently, however, the periodontal tissues of the incisors, after eight days of hipofunction, showed stronger immunoreactivity, particularly with CSF-1, as compared with incisors under normal and hiperfunctional conditions. The results suggest that this molecular ¿cascade¿, may be related with the enlargement of the rodent incisor eruptive pathway, since these teeth grow for a long period of animal¿s life
Doutorado
Histologia e Embriologia
Doutor em Biologia Buco-Dental
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Lue, Hui-wen. "LIV-1 Promotes Prostate Cancer Epithelial-to-Mesenchymal Transition and Metastasis Through HB-EGF Shedding and EGFR-mediated ERK Signaling." Digital Archive @ GSU, 2012. http://digitalarchive.gsu.edu/biology_diss/115.
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LIV-1, a zinc transporter, is an effector molecule downstream from soluble growth factors. This protein has been shown to promote epithelial-to-mesenchymal transition (EMT) in human pancreatic, breast, and prostate cancer cells. Despite the implication of LIV-1 in cancer growth and metastasis, there has been no study to determine the role of LIV-1 in prostate cancer progression. Moreover, there is no clear delineation of the molecular mechanism underlying LIV-1 function in cancer cells. In this study, we found increased LIV-1 expression in a progresssive manner in benign, PIN, primary and bone metastatic human prostate cancer. We characterized the mechanism by which LIV-1 drives prostate cancer EMT in an androgen-refractory human prostate cancer cell (ARCaP) bone metastasis model. LIV-1, when overexpressed in ARCaPE cells (derivative cells of ARCaP with epithelial phenotype), promoted EMT irreversibly. LIV-1 overexpressed ARCaPE cells had elevated levels of HB-EGF and matrix metalloproteinase (MMP) 2 and MMP 9 proteolytic enzyme activities, without affecting intracellular zinc concentration. The activation of MMPs resulted in the shedding of heparin binding-epidermal growth factor (HB-EGF) from ARCaPE cells, eliciting constitutive epidermal growth factor receptor (EGFR) phosphorylation and its downstream extracellular signal regulated kinase (ERK) signaling. Further investigation of the HB-EGF promoter revealed that both Stat3 and AP-1 controlled HB-EGF promoter activity. Ectopic LIV-1 overexpression induced AP-1 and Stat3 activation. Blockade of both Stat3 and AP-1 by specific inhibitors or dominant negative expression vectors diminished the HB-EGF promoter activity induced by LIV-1 overexpression. These results suggest that LIV-1 is involved in prostate cancer progression as an intracellular target of growth factor receptor signaling which promotes EMT and cancer metastasis. LIV-1 could be an attractive therapeutic target for the eradication of pre-existing human prostate cancer and bone and soft tissue metastases.
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Liu, Xiaoying. "Molecular mechanisms of myofibroblast differentiation and the role of TGF beta 1, TNF alpha, and thrombin signal transduction." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1236711907.
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Mahtouk, Karène. "Syndecan-1 : un partenaire indispensable des membres de la famille EGF dans le myélome multiple." Montpellier 2, 2005. http://www.theses.fr/2005MON20107.
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Overeem, Kathie. "Retrograde signalling within fear neurocircuitry: Nitric oxide signalling from the lateral nucleus of the amygdala regulates thalamic EGR-1 mediated alterations of presynaptic protein levels during auditory fear conditioning." Thesis, University of Canterbury. Psychology, 2009. http://hdl.handle.net/10092/3212.
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Previous research has shown that nitric oxide signalling in the lateral nucleus of the amygdala is required for the consolidation of Pavlovian conditioned fear. Given the evidence that nitric oxide can act as a retrograde signalling molecule in in vitro models of memory consolidation the question arises whether this is also occurring within behavioural memory models? Using auditory fear conditioning this research shows that nitric oxide does indeed act as retrograde signalling molecule in the fear system. Its synthesis in the lateral nucleus of the amygdala regulates conditioning induced expression of the immediate early gene early growth response gene 1 (EGR-1) in cells of the auditory thalamus that project to the lateral nucleus of the amygdala. The regulation of EGR-1 expression by the lateral nucleus of the amygdala was proven to be dependent on amygdala-based cellular excitation, nitric oxide synthesis and NR2B-NMDA receptor activation but not ERK/MAPK activity. Using an EGR-1 antisense oligonucleotide to prevent training induced EGR-1 expressions in the auditory thalamus it was shown that this gene upregulation is necessary for the consolidation of conditioned fear. Finally, inhibition of EGR-1 upregulation in the auditory thalamus was proven to impair conditioning induced increases in the presynaptic proteins synaptophysin, and synapsin II and II back in the lateral nucleus of the amygdala. Overall, the results of this dissertation have shown that nitric oxide acts as a retrograde messenger in a mammalian memory system by modulating gene expression in presynaptic cells. This modulation of gene expression serves to increase levels of presynaptic proteins back at the origin of nitric oxide synthesis. This supports the long standing doctrine that nitric oxide acts as a retrograde signalling molecule to coordinate presynaptic changes associated with memory formation.
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Gaggioli, Cédric. "Etude de l'expression de la fibronectine dans les cellules de mélanome : rôle de la voie de signalisation des MAP kinases ERK et du facteur de transcription Egr-1." Paris 7, 2005. http://www.theses.fr/2005PA077021.
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Spasevska, Ivana. "The role of EGR-1 and calcium influx in the antitumor activity of anti-CD20 monoclonal antibodies." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSE1304/document.
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Les anticorps monoclonaux (AcM) anti-CD20 sont essentiels pour le traitement du lymphome non hodgkinien et de la leucémie lymphoïde chronique (LLC). Les AcM agissent soit en activant directement la signalisation apoptotique dans les cellules cibles, soit via le système immunitaire. Dans une étude préclinique, nous avons montré que le traitement avec AcM anti-CD20, rituximab et GA101, induit l'expression de la protéine early growth response 1 (EGR-1) (Dalle et al., 2011). EGR-1 est un facteur de transcription régulé par le calcium (Ca2+) et CD20 est impliqué dans la régulation du flux calcique transmembranaire. Nous avons donc étudié le rôle d'EGR-1 et du flux Ca2+ dans l'activité cytotoxique des AcM anti-CD20. Nous avons montré qu'EGR-1 est rapidement induit suite à l'exposition au rituximab et à GA101. La baisse de l'expression d'EGR-1 par shRNA a supprimé l'effet cytotoxique du GA101 à la fois in vitro et in vivo, indiquant qu'EGR-1 est requis pour la mort cellulaire médiée par CD20. De plus, la surexpression d'EGR-1 augmente la sensibilité au GA101 in vitro et in vivo. En outre, nos résultats indiquent que les AcM anti-CD20 induisent un flux Ca2+. Le blocage du flux Ca2+ par inhibiteurs de canaux calciques (ICC) a aboli l'induction d'EGR-1 ainsi que l'efficacité du GA101 in vivo et ex vivo dans des échantillons de LLC. Plus important, nos données indiquent que les patients recevant des ICC ont une moins bonne réponse au traitement par les AcM anti-CD20. En conclusion, nous avons identifié EGR-1 comme potentiel biomarqueur pour prédire la réponse à la thérapie anti-CD20 et démontré que les ICC ont un impact négatif sur l'efficacité des AcM anti-CD20 chez les patientsAnti-CD20 monoclonal antibodies (mAbs) are an essential component of the treatment of patients with non-Hodgkin's lymphoma and chronic lymphocytic leukemia (CLL). They mediate their antitumor effects by activating the immune system or by direct apoptotic signaling in target cells. In a previous preclinical study, we showed that treatment with anti-CD20 mAbs, rituximab and GA101, resulted in upregulated expression of early growth factor 1 (EGR-1) (Dalle et al. 2011). EGR-1 is a calcium (Ca2+) regulated transcription factor and CD20 is hypothesized to regulate transmembrane Ca2+ flux. Therefore, we aimed to assess the role of EGR-1 and Ca2+ flux in the cytotoxic activity of anti-CD20 mAbs. We have shown that EGR-1 expression is rapidly upregulated in CD20+ cells following rituximab and GA101 exposure. Decreasing EGR-1 expression by shRNA abolishes the direct cytotoxic effect of GA101 both in vitro and in vivo, indicating that EGR-1 is required for CD20-mediated cell death. Additionally, the overexpression of EGR-1 enhances the cytotoxic activity of GA101 both in vitro and in vivo. Furthermore, our results indicate that anti-CD20 mAbs induce calcium influx. Blocking the Ca2+ flux with calcium channel blockers (CCB) abolishes EGR-1 induction and impaires the GA101 efficacy in vivo and ex vivo in CLL blood samples. More importantly, our data indicate that patients receiving CCBs and anti-CD20 therapy have worst progression free survival and overall survival. In conclusion we have identified EGR-1 as a potential biomarker to predict response to anti-CD20 therapy. We demonstrated that co-treatement with CCBs negatively impacts the outcome of patients receiving anti-CD20 mAbs
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Tur, Arlandis Gema. "Transcriptional regulation of egr-1 gene in murine cells. Towards the understanding of the role of chromatin." Doctoral thesis, Universitat de València, 2007. http://hdl.handle.net/10803/9545.
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Eukaryotic gene expression is a highly regulated process that has to ensure the right cellular response to any type of stimulus. Nevertheless, chromatin structure, despite the fact of being dinamic, imposes certain contraints to this regulation. To solve this restrictions, cells have organized the recruitment of chromatin modifying enzymes and ATP-dependent chromatin remodelling enzymes. The first class of enzymes are responsible for the covalent modifications of histones which alter the global charge of the histones and also serve to recruit specific co-factors to the chromatin. The second group of enzymes uses the energy from ATP hydrolisis to modify the interactions DNA-histones, therefore increasing the nucleosomal DNA accesibility to the transcriptional machinery. The understanding of the mechanisms that the cell uses to regulate expression of an immediate-early gene such as egr-1, are very important, not only for the basic molecular knowledge but also for the understanding of different pathologies. The coordinated action of the signalling pathways, the union of transcriptional factors and enzymatic complexes that act over the chromatin is crucial for the right interpretation of the genetic code, which is specific for each gene under study. In the case of egr-1, treating MLP29 cells with TPA activates expression after 5 min of treatment, has a peak around 15 and 30 min, and decreases subsequently to be undetectable at 180min after the treatment. This induction takes place through the MAP and p38 kinase cascades which also act phosphorylating the promoter transcriptional factors ELK1 and CREB. Chromatin immunoprecipitation experiments (ChIP), suggest that egr-1 is a gene "ready to be expressed", as the RNAPol II and the SRF, ELK1, CREB and SP1 transcriptional factors are already present in the basal state of the gene. During the induction process SP1 leaves the promoter and EGR-1, NAB1 and NAB2 are recruited. In the same manner, ChIP experiments have detected the presence of two HDAC complexes implicated in egr-1 repression (mSIN3A and HDAC3-NcoR) and the presence of two HAT complexes (CBP, with a possible role as maintaining the basal acetylation levels and GCN5 which putative role would favour the induction process). The presence of these enzymes has been correlated with a general increase in the levels of acetylation of histone H3 and H4 by immunoprecipitating against specific histone modifications. Additionally, experiments of Micrococcal nuclease protection have suggested the existence of three positioned nucleosomes in egr-1 promoter and also the movement of the more proximal to the transcription start during the induction process. That nucleosomal mobility has been related to the presence of the ATPase BRM and BRG1 in the promoter of the gene and also with specific increases in the acetylation levels of the three nucleosomes as revealed by mononuclesomal ChIP experiments. Moreover, to study the biological effect of the lack of EGR1, it has been designed a siRNA sequence that is able to decrease egr-1 expression up to a 70%, and which biological activity has been shown by a decrease in nab2 (EGR1 target gene) expression of 40%. Lastly, the interconnection between these results has allowed us to hypothesize a model for the epigenetic regulation of egr-1 gene in murine cells treated with TPA.La regulación de la expresión génica en eucariotas se encuentra condicionada por la estructura de la cromatina. Por ello, la comprensión de los mecanismos que utiliza la célula para regular la expresión de un gen inmediato-temprano, como egr-1, es de gran importancia tanto para el conocimiento básico molecular como para la compresión de diferentes patologías. El tratamiento de células MLP29 con TPA activa la expresión del gen egr-1 a los 5 min., alcanza un pico entre los 15 y 30 min. y deja de ser detectable a los 180 min. Dicha inducción, se produce a través de las cascadas de quinasas MEK y p38, que además fosforilan a los factores ELK1 y CREB, presentes en el promotor del gen. Experimentos de inmunoprecipitación de cromatina (ChIP), indican que egr-1 posee la RNAPol II y los factores SRF, ELK1, CREB y SP1 unidos al promotor en el estado basal. Durante la inducción, SP1 se libera y EGR1, NAB1 y NAB2 son reclutados. Asimismo, experimentos de ChIP han detectado la presencia en el promotor de dos complejos HDAC (mSIN3A y HDAC3-NCoR) y de dos complejos HAT (CBP y GCN5). Estos enzimas se han correlacionado con un incremento general en los niveles de acetilación de las histonas H3 y H4 mediante ChIP con anticuerpos específicos. Además, experimentos de protección frente a digestión con nucleasa de micrococo sugieren la existencia de 3 nucleosomas posicionados en el promotor de egr-1 así como el movimiento del más próximo al inicio de la transcripción durante el proceso de inducción. Dicha movilidad nucleosomal se ha correlacionado mediante ChIP con la presencia de las ATPasas BRM y BRG1 en el promotor del gen y con incrementos específicos de acetilación de los tres nucleosomas, estudiados mediante ChIP de mononucleosomas. El efecto biológico de EGR1 se ha estudiado mediante RNA de interferencia capaz de producir una disminución del nivel de expresión de egr-1 de un 70% y la inhibición parcial de genes diana como es el caso de nab2. Finalmente, la interconexión de estos resultados nos ha permitido hipotetizar un posible mecanismo de regulación epigenética del gen egr-1 en células MLP29 inducidas por TPA.
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Rademacher, Svenja [Verfasser], and Thomas [Akademischer Betreuer] Dresselhaus. "EGG CELL 1 function and stability during double fertilization in Arabidopsis thaliana / Svenja Rademacher. Betreuer: Thomas Dresselhaus." Regensburg : Universitätsbibliothek Regensburg, 2011. http://d-nb.info/1023398745/34.
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DIAS, CARLA R. de B. R. "Estudo de marcação dos anticorpos monoclonais IOR-CEA-1 e IOR-EGF/R3 com sup(99m)Tc." reponame:Repositório Institucional do IPEN, 2005. http://repositorio.ipen.br:8080/xmlui/handle/123456789/11337.
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Made available in DSpace on 2014-10-09T12:50:50Z (GMT). No. of bitstreams: 0Made available in DSpace on 2014-10-09T13:58:08Z (GMT). No. of bitstreams: 1 11096.pdf: 7071913 bytes, checksum: f0395995edaa69e463b5e5407a40c10c (MD5)
Dissertacao (Mestrado)
IPEN/D
Instituto de Pesquisas Energeticas e Nucleares - IPEN/CNEN-SP
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Rademacher, Svenja Verfasser], and Thomas [Akademischer Betreuer] [Dresselhaus. "EGG CELL 1 function and stability during double fertilization in Arabidopsis thaliana / Svenja Rademacher. Betreuer: Thomas Dresselhaus." Regensburg : Universitätsbibliothek Regensburg, 2011. http://d-nb.info/1023398745/34.
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Bishop, Kenneth D. "Egr-2 and PD-1 Are Required for Induction and Maintenance of T Cell Anergy: A Dissertation." eScholarship@UMMS, 2005. https://escholarship.umassmed.edu/gsbs_diss/354.
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The prevalence of diabetes is approaching epidemic proportions worldwide. There is currently no cure for type 1 diabetes, and successful treatment requires constant monitoring of blood sugars and use of exogenous insulin to prevent hyperglycemia. Diabetes will be curable when pancreatic β-islet cells can be transplanted into diabetes patients without requiring long-term immunosuppression. This will require learning more about the induction of functional tolerance, a state that maintains the competence of the immune system to most antigens but protects graft-specific antigens from immune rejection, permitting transplantation. One known mechanism of peripheral tolerance is T cell anergy, a phenotype of hypo-reponsiveness in CD4+ T cells. The focus of this thesis is a description of factors shown to be specific to the induction and maintenance of T cell anergy, whose loss reverses the anergic phenotype, restoring the ability of the cells to proliferate in response to antigen. The first of these is Egr-2, a zinc-finger transcription factor, whose presence is required for the induction of anergy induced in T cell clones by TCR stimulation in the absence of costimulation. Egr-2 is shown to be important to anergy induction but not anergy maintenance. In contrast, a negative costimulation receptor, PD-1, is shown to be necessary for the maintenance of anergy. It is possible that learning more about the genetic factors that orchestrate T cell anergy will prove useful in the development of tolerance-based protocols for organ and tissue transplantation without the use of long-term immunosuppression.
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Chakrabarti, Arindam. "PKR DEPENDENT UPREGULATION OF IMMEDIATE EARLY GENES AND ANTI-INFLAMMATORY CYTOKINE IL-10." Kent State University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=kent1176136341.
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Gregg, Jennifer L. "EGF-Mediated Regulation of EGR1 in Prostate Cancer Cells." Kent State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=kent1283287954.
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Zeitz, Julia. "Der Begriff der Beihilfe im Sinne des Artikels 87 Abs. 1 EG-Vertrag /." Berlin : Logos-Verl, 2005. http://www.gbv.de/dms/spk/sbb/recht/toc/481289925.pdf.
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Cho, Moonjeong. "Attenuation of Egr-1 induced apoptosis by inhibition of p53 and its implications as potential inhibitor of Alzheimer's Disease." Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=123316.
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The mechanism in which neurodegeneration occurs in Alzheimer's disease (AD) is unclear but apoptosis is a conjectured trigger in multiple studies. Moreover, studies with post-mortem brains of AD patients showed increased levels of early growth response-1 (Egr-1), particularly in regions primarily manifested with AD pathology, such as hippocampus and frontal cortex. However, its pathological significance is unknown. Egr-1 is a critical transcription factor involved in various biological processes which include apoptosis, cell proliferation and cell survival. Depending on cellular context and al stimuli, Egr-1 regulates the transcription of different target genes controlling different biological functions. During apoptosis, Egr-1 either transactivates tumour suppressors, such as p53 and Bax, or transrepresses proto-oncogene Bcl-2 to promote apoptosis. Egr-1 also transcriptionally regulates cyclin D1 (CCND1), a key regulator of G1 phase progression of the cell cycle that is essential for re-entry into the cell cycle and mediation of apoptosis. However, in neuronal apoptosis, direct targets of Egr-1 remain to be elucidated. Therefore, the following apoptotic genes were examined using models either overexpressing or suppressing Egr-1: Bcl-2, CCND, and p53. It is shown that Egr-1 upregulates p53 gene, along with direct transcriptional target genes of p53, including Bax and the promyelocytic leukaemia (PML). In order to investigate whether Egr-1-induced apoptosis occurs via p53, p53 activity was abrogated using the p53 inhibitor pifithrin-α (PFTα). I report a mitigation of Egr-1-induced cellular death. Moreover, because Egr-1-regulated apoptotic gene expression is also known to change in post-mortem brain of AD patients, we again examined the expression of Bcl-2, CCND1, and p53, in the triple transgenic (3xTg) AD mouse model. These mice display both tau and amyloid pathology. This study shows an age-dependent increase in both p53 protein level and gene expression in the 3xTg-AD brain compared to the control group. These findings in conjunction with a rise in Egr-1 gene expression in AD, suggest their possible implication in neurodegenerative processes.Le mécanisme dans lequel survient la maladie de l'Alzheimer (MA) est incertain, mais l'apoptose est une hypothèse d'après de nombreuses recherches. Plus encore, des études ayant faites des autopsies du cerveau des patients atteints d'Alzheimer ont démontré une plus grande abondance de la protéine early growth response-1 (Egr-1), plus particulièrement dans les régions où se manifestent principalement la pathologie de cette maladie, soit dans l'hippocampe et le cortex frontal. Par contre, son importance pathologique est inconnue. Le Egr-1 est un facteur crucial pour la transcription, qui est impliquée dans divers procédés biologiques comme l'apoptose, la prolifération cellulaire et la survie. Selon le contexte de la cellule et des stimuli physiopathologiques, le Egr-1 régularise la transcription des différents gènes cibles pour exécuter des différentes fonctions biologiques. Lors de l'apoptose, le Egr-1 transactive des gènes suppresseurs de tumeur comme p53 et Bax, ou la transrepression du proto-oncogène Bcl-2 a lieu pour favoriser l'apoptose. Le Egr-1 régule également la transcription de la cycline D1 (CCND1), un régulateur clé de la progression de la phase G1 du cycle cellulaire, qui est essentiel pour rentrer dans le cycle cellulaire et la médiation de l'apoptose. Cependant, l'apoptose neuronale, la cible principale du Egr-1, reste à être élucidée. Donc, c'est pourquoi les gènes apoptotiques suivants ont été examinés en utilisant des modèles où le Egr-1 était surexprimé ou repressé: Bcl-2, CCND1, et p53. Nous démontrons que le Egr-1 accroit le gène p53, ainsi que les gènes cibles transcriptionnels du p53, dont Bax et la leucémie promyélocytaire (PML). Afin de déterminer si l'apoptose induit par Egr-1 était à cause de l'activité de p53, l'activité de p53 a été abrogée en utilisant pifithrin-α (PFTα), l'inhibiteur de p53. Nous avons découvert une atténuation de la mort cellulaire induite par Egr-1. Plus encore, puisque les expressions des gènes apoptotiques régulés par Egr-1 sont aussi connus pour changer dans les cerveaux (des patients atteints de la MA) qui ont été autopsiés, j'ai examiné les mêmes gènes apoptotiques (Bcl-2, CCND1 et p53) que j'ai testés avec le modèle Egr-1 utilisant des souris triples transgéniques (3xTG) qui sont connues pour imiter et développer étroitement la neuropathologie des patients atteints de la MA. Cette étude démontre une augmentation de la protéine p53, qui dépend de l'âge, ainsi qu'une augmentation de l'expression du gène p53 dans les cerveaux 3xTG atteints de la MA par rapport au groupe témoin. Ces résultats en liaison avec une augmentation du niveau de gène Egr-1 dans la MA suggèrent leur possible implication dans les processus neurodégénératifs.
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Falk, Matthias Ulrich. "Die Rolle der Kinasen ERK1 und ERK2 sowie des Transkriptionsfaktors Egr-1 in der Genetik des kindlichen Asthma bronchiale." [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:25-opus-60433.
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Leopold, Anders. "Rechtsprobleme der Zusammenarbeit im Netzwerk der Wettbewerbsbehörden nach der Verordnung (EG) Nr. 1/2003 /." Baden-Baden : Nomos-Verl.-Ges, 2006. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=015042889&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.
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Helvaci, Elif. "The Impact Of Perceived Parental Control On Internalization And Ego-depletion." Master's thesis, METU, 2010. http://etd.lib.metu.edu.tr/upload/12612821/index.pdf.
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The aim of the current study is to examine the potential parenting factors and mediating mechanisms that lead to ego-depletion within the framework of Self-Determination Theory. Previous research has suggested that whereas behaviourally controlling and autonomy-supportive parenting contributes to the development of autonomous motivation, psychologically controlling parenting leads to introjected motivation for self-regulation. Moreover, recent studies have shown that as compared to introjected regulation, autonomous regulation depletes less ego-resource. Thus, it was expected that parental psychological control positively, but behavioural control negatively, affects ego-depletion via controlled regulation style. In the first study, university students (N = 179) completed three groups of measures assessing parenting behaviours, motivation type of self-regulation, and state self-control capacity. The results of SEM analysis partially supported the proposed mediational model. Whereas both maternal and paternal psychological control indirectly predicted self-control capacity corresponding higher levels of ego depletion via controlled regulation, parental behavioural control did not have direct or indirect effect on self-control capacity. In the second study, the same hypotheses were tested experimentally on a group of participants (N = 91) from the first study by exposing them either an upsetting or a funny video condition that requires emotional control. Results revelaled that perceived high levels of maternal psychological control and low levels of paternal behavioural control make individuals more vulnerable to ego-depletion under emotional control. Furthermore, those with high introjected motivation for emotion-control were relatively resistant to ego-depletion. Findings were discussed considering the practice effect of self-control, implications of diverging parenting behaviours and cultural factors.
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Séry, Quentin. "Résistance au témozolomide dans le glioblastome multiforme : rôle de l'induction du HBEGF." Nantes, 2014. http://archive.bu.univ-nantes.fr/pollux/show.action?id=362effa8-bfad-466c-a23f-cca177c08184.
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Le glioblastome multiforme (GBM) est une tumeur cérébrale hautement réfractaire au traitement. Ces dernières années l'utilisation du témozolomide (TMZ), un agent alkylant, couplé à la radiothérapie a permis d'augmenter la survie des patients mais celle-ci reste en moyenne inférieure à un an. Au cours de cette thèse, nous nous sommes intéressés dans un premier temps au rôle des protéines pro-apoptotiques Bax et Bak dans l'apoptose induite par le TMZ. Nous avons pu mettre en évidence un rôle proéminent de l'axe Mcl-1/Bak dans l'induction de l'apoptose en réponse au TMZ. Le récepteur à tyrosine kinase EGFR est impliqué dans l'oncogenèse des GBMs primaires (35-45% d'amplification) mais aussi dans la résistance au traitement. Dans un second temps nous avons donc analysé l'expression de ligands d'EGFR et mis en évidence une surexpression du HBEGF en réponse au TMZ dans deux lignées n'exprimant pas l'enzyme de réparation MGMT principal facteur de résistance au TMZ. Contre-intuitivement le HBEGF n'a pas de rôle dans la résistance mais s'est révélé être impliqué dans la dégradation de Mcl-1 induite par le TMZ. Ce rôle est indépendant de l'activité de l'EGFR. Nos résultats suggèrent l'implication de la protéine cochaperonne BAG-1 et de la déubiquitinase USP9X dans ce mécanisme. Globalement, nos résultats identifient Bak comme l'inducteur principal de l'apoptose après un traitement par le TMZ, proposent un nouveau mécanisme de dégradation de Mcl-1 et mettent en avant un rôle du HBEGF dans la réponse au traitement indépendamment de son récepteur EGFR. De plus, ils identifient BAG-1 comme partenaire privilégié du HBEGF et l'implique dans la régulation de Mcl-1 par sa déubiquitinase USP9XGlioblastoma multiforme (GBM) is a cerebral tumor highly refractory to treatment. Over the past years the akylating agent temozolomide (TMZ) associated with radiotherapy has improved the survival of patients but overall survival is still inferior to one year. During this thesis, we first examine the role of pro-apoptotic proteins Bax and Bak in TMZ-induced apoptosis and highlighted the major role of Mcl-1/Bak axis in TMZ mediated apoptosis. The tyrosine kinase receptor EGFR is implicated in primary GBMs oncogenesis (35-45% of amplification) and in resistance to treatment. Then we analyzed expression of EGFR ligands and founded an up-regulation of HBEGF in response to TMZ in two cell lines without expression of the repair enzyme MGMT the main resistance factor to TMZ. Counter-intuitively HBEGF is not involved in resistance but in TMZ-induced Mcl-1 degradation. This role is independent of EGFR activity. Implication of HBEGF in Mcl-1 degradation has no effect on caspases activity after TMZ treatment. Among the few known intracellular partners of HBEGF the chaperone protein BAG-1 is implicated in Mcl-1 expression maintenance. Indeed BAG-1 regulates Mcl-1 through its deubiquitinase USP9X. TMZ enable HBEGF/BAG-1 interactions and disable USP9X/Mcl-1 interactions. Our results then identify Bak as the main apoptosis inducer in response to TMZ, propose a new mechanism for the induced degradation of Mcl-1 and highlight a new role of HBEGF independently of its receptor EGFR. Moreover they identify BAG-1 as a favored partner of HBEGF and implicate it in Mcl-1 regulation via its deubiquitinase USP9X
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Granet, Corinne. "Mécanismes d'adaptation de cellules ostéoblastiques Ros17/2. 8 aux variations des contraintes mécaniques dans des modèles de micro-gravité simulée et de déformation du support de culture : implication des facteurs de transcription : AP-1, Egr-1, NF-kB." Saint-Etienne, 2000. http://www.theses.fr/2000STET006T.
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Bührle, Folko. "Gründe und Grenzen des "EG-Beihilfenverbots" : Art. 87 Abs. 1 EG-Vertrag - eine europäische Norm im Spannungsfeld von ökonomischer Rationalität und staatlichem Gestaltungsanspruch /." Tübingen : Mohr Siebeck, 2006. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=014885727&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.
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Coskan, Canan. "The Effects Of Self-control And Social Influence On Academic Dishonesty: An Experimental And Correlational Investigation." Master's thesis, METU, 2010. http://etd.lib.metu.edu.tr/upload/12612678/index.pdf.
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The present study aimed to integrate situational and dispositional perspectives on the investigation of unethical and dishonest behavior through an experimental and a correlational study. More explicitly, the current study explored the effects of state self-control and social influence on cheating, and investigated the trait self control and conformity as predictors of academic dishonesty.
Two preliminary studies were conducted. First, a pilot study with 230 undergraduate students was conducted to assess the reliability of the Turkish versions of the four scales intended to measure the constructs of interest. All four scales were found to have sufficient reliabilities. A second preliminary study was conducted to observe and to ameliorate the effects of two manipulations constructed for the main study, namely the rewriting task (depletory versus neutral) and the norm induction (deciding to cheat, not to cheat or to meet with a friend after the study). The main study was conducted with 87 undergraduate students. Correlational results underlined the importance of low self-control and high susceptibility to social influence as predictors of past behavior of academic dishonesty. Experimental results revealed that first, groups
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Kramer, Elizabeth L. "Role of the EGFR Pathway in Lung Remodeling and Disease." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1250206890.
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Rueda, André Veloso Lima. "O enriquecimento ambiental inibe a sensibilização comportamental ao etanol em camundongos: efeitos sobre o Egr-1 e a sinalização do BDNF." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-12082011-155938/.
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O uso de drogas de abuso pode levar a alterações neuroplásticas duradouras no encéfalo, entre elas a sensibilização comportamental (SC), um fenômeno relacionado à dependência. O enriquecimento ambiental (EA) permite estudar a influência do ambiente na resposta a diversas manipulações, entre elas o tratamento com drogas de abuso. O objetivo deste trabalho foi avaliar o efeito do EA sobre a SC ao etanol, e sobre a expressão de proteínas envolvidas nas respostas às drogas de abuso: BDNF, TrkB e Egr-1. Para tanto, camundongos foram expostos ao EA, e então tratados repetidamente com uma dose baixa (1,8 g/kg) de etanol. Outros grupos foram submetidos ao protocolo de SC e posteriormente expostos ao EA. O EA protegeu os animais de desenvolverem a SC ao etanol, bem como promoveu sua reversão. O EA diminuiu os níveis de BDNF no córtex pré-frontal e de TrkB no hipocampo, e aumentou a expressão de Egr-1 no córtex insular. O EA pode ser considerado uma estratégia útil para a reversão dos efeitos da SC, que está associada à fissura e a episódios de recaídas na dependência.The use of addiction drugs can lead to long-term neuroplastic changes on the brain, such as behavioral sensitization (BS), a phenomenon related to addiction. Environmental enrichment (EE) is a strategy used to study the environmental influence on the response to several manipulations, including the treatment with addiction drugs. The aim of this work was to evaluate the effects of EE on the BS to ethanol and on the expression of proteins related to the response to drugs of abuse, as BDNF, TrkB and Egr-1. Thus, mice were exposed to EE and then repeatedly treated with a low dose (1.8 g/kg) of ethanol. Other group of mice was first submitted to the BS protocol and then exposed to EE. EE protected the mice from developing the BS to ethanol, and promoted its reversion. EE decreased BDNF levels in the prefrontal cortex and TrkB in the hippocampus, and increased Egr-1 expression in the insular cortex. EE can be considered and useful strategy to block BS effects, a phenomenon related to craving and relapse.
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Yochiy, Angélica. "Expressão dos genes de ativação imediata c-fos e egr-1 em encéfalos de ratos submetidos ao modelo do desamparo aprendido." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/47/47135/tde-26072010-143609/.
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O desamparo aprendido (DA) corresponde à dificuldade de aprendizagem operante em função de exposição prévia a choques incontroláveis. Esse efeito vem sendo proposto como modelo animal de depressão e também defendido por alguns pesquisadores como modelo animal para o transtorno de estresse pós-traumático (TEPT). O objetivo do presente trabalho foi examinar a ativação dos genes c-fos e egr-1 em áreas do encéfalo de ratos submetidos ao tratamento que induz o desamparo aprendido, priorizando estruturas consideradas funcionalmente importantes para os distúrbios de aprendizagem, como a amígdala (AMI), o hipocampo (HIP) e o córtex pré-frontal medial (CPFm). Considerado importante para o desenvolvimento do desamparo aprendido por alguns autores, o núcleo septal lateral (NSL) também foi analisado. No estudo, ratos machos Wistar adultos, sujeitos do grupo Incontrolável (INC), após período de adaptação ao ambiente laboratorial, receberam 60 choques inescapáveis de 1,0 mA, 10 segundos de duração, ministrados nas patas a intervalos médios de 1 minuto. Após 24 horas, estes animais e os controles ingênuos (ING), que não receberam choques no tratamento, foram submetidos à contingência de fuga. Critérios de aprendizagem previamente estabelecidos foram aplicados para selecionar os animais do grupo ING que aprenderam, e para separar os sujeitos do grupo INC nos subgrupos dos animais que não aprenderam (DES) e dos que aprenderam normalmente (NDE). Grupos controle sem adaptação e sem choque (BIO), ou com adaptação e sem choque (ADA), também foram manipulados. Após o teste de aprendizagem, os animais foram anestesiados, perfundidos, e seus encéfalos extraídos. Os cortes dos encéfalos foram tratados para imunoperoxidase para revelar as proteínas Fos e Egr-1. Os resultados evidenciaram características distintas de expressão dos genes c-fos e egr-1 nas diferentes estruturas. Foi observado um aumento na imunorreatividade para Fos nas áreas CA1 do HIP e CPFm para o grupo ING, e uma redução do marcador Fos no CPFm do grupo DES se comparado ao grupo NDE. Um aumento na imunorreatividade para Egr-1 foi evidenciado no giro denteado (GD) do HIP do grupo DES em relação a todos os grupos, à exceção do grupo ING. Na região central da AMI o aumento para Egr- 1 ocorreu no grupo DES em relação ao grupo ING, e na região basolateral, entre o grupo DES e os grupos BIO e ING. Os coeficientes de correlação de Pearson mostraram covariação entre os dados das duas regiões da AMI e entre os dados do GD para Egr-1 e NSL para Fos e Egr-1. Também foi evidenciada uma maior correlação entre os dados dos dois marcadores no grupo DES, seguido do NDE e do ING, nesta sequência. Os dados indicam que circuitos neurais relacionados à aprendizagem e memória estão envolvidos no desenvolvimento do desamparo aprendidoThe learned helplessness (LH) phenomenon corresponds to difficulties in operant learning as a result of previous exposure to uncontrollable shocks. This effect has been suggested as an animal model of depression and posttraumatic stress disorder (PTSD). The purpose of this work was to examine the activation of c-fos and egr-1 genes in brain areas of rats exposed to treatment which induces the LH behavior, especially in some structures recognized as functionally important to learning disorders, such as the amygdala (AMI), the hippocampus (HIP), and the medial prefrontal cortex (mPFC). Cited as important to LH development the lateral septal nucleus (LSN) was also examined. In the experiment, adult male Wistar rats from the uncontrollable group (INC), after a 3-day exposure to the experimental conditions, received 60 inescapable 1.0 mA footshocks lasting 10 seconds each, applied at an average interval of 1.0 minute. After 24 hours, these animals and the naive controls (ING), which did not receive footshocks during treatment, were tested in a shuttlebox. Previously established criteria were applied to select the ING animals that learned the escape response, and also to sort the INC animals into nonlearning (DES) and learning (NDE) subgroups according to their performance during the escape test. Subjects not exposed to adaptation or footshocks (BIO), and subjects adapted but not exposed to footshocks (ADA) were also manipulated. All animals received anesthesia and after transcardiac perfusion had their brains removed, sectioned and immunohistochemically treated to reveal Fos and Egr-1 proteins. The results showed distinct attributes for c-fos and egr-1 gene expression in the brain structures examined. Data analysis revealed significantly higher Fos immunoreactivity in the HIP CA1 and mPFC in the ING group than in the other groups. A decrease was detected in Fos-positive nuclei in the DES group mPFC compared with the NDE group. An increase in the Egr-1 positive nuclei was found in the HIP dentate gyrus (DG) in the DES group compared with all the groups, except the ING group. An increment in Egr-1 imunoreactivity was also detected in the central AMI in the DES group in relation to ING group, and in the basolateral AMI in the DES group against the BIO and ING groups. Pearsons correlation test indicated covariation between data from central and basolateral AMI regions. A high correlation coefficient was found between data from DG for Egr-1 and from NSL for both Fos and Egr-1. A high correlation was observed between the two markers for the DES group, followed by the NDE and ING groups, in that sequence. The results suggest that the neural circuits underlying memory and learning are implicated in the development of the LH effect
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Bjurström, Gaëlle, and Åsa Coutts. "Begreppet skada på konkurrensen enligt artikel 8 i Rådets förordning (EG) nr 1/2003 : - En tolkningsfråga." Thesis, Linköpings universitet, Affärsrätt, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-129282.
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Denna uppsats undersöker tillämpningen av artikel 8 i Rådets förordning (EG) nr 1/2003 av den 16 december 2002 om tillämpning av konkurrensreglerna i artiklarna81 och 82 i fördraget (härefter ”Förordningen”). Enligt nämnda artikel får interimistiska åtgärder tillgripas för att motverka en överhängande risk för allvarlig och irreparabelskada på konkurrensen. I detta sammanhang anser Konkurrensverket att begreppetskada på konkurrensen behöver klargöras, och undrar om det kan likställas medbegreppet konkurrensskada. Därför har vi definierat begreppen i förhållande till varandra för att kunna dra slutsatser angående tillämpningen av artikel 8 i Förordningen. Vår utredning visar att konkurrensskada är ett snävt begrepp som syftar på en ren förmögenhetsskadasom drabbar individuella skadelidande på grund av en konkurrensrättsligöverträdelse. Begreppet utgår i allra högsta grad från ett individperspektiv ochkan, men behöver inte, sammanfalla med skadan som åsamkas konkurrensen, ekonomineller samhället. Skada på konkurrensen däremot, är ett allomfattande begrepp somåsyftar den allmänna skadan som åsamkas ekonomin i stort på grund av en överträdelseav konkurrensrätten. Trots att begreppet är allmänt hållet och öppet för fri tolkning av rättstillämparen, ställs specifika krav för förordnande av interimistiska åtgärder enligt artikel 8 i Förordningen, nämligen en prima facie konkurrensrättslig överträdelse som medför en risk för allvarlig och irreparabel skada på konkurrensen. Risken för att konkurrensenskadas måste preciseras på ett konkret och trovärdigt sätt och allvarlighetskravetinnebär till exempel att en konkurrent riskerar att försättas i konkurs. För attvara irreparabel får inte en skada kunna läkas av ett senare beslut av konkurrensmyndigheten. Skadan får inte heller endast vara av ekonomisk art. Slutsatsen är att det ställs höga krav för tillämpningen av artikel 8 i Förordningen,vilket kan förklara den nuvarande avsaknaden av praxis. Behovet för interimistiskaåtgärder anses dock vara stort, inte minst på grund av de långa handläggningstiderna i konkurrensmål. Därför anser vi att konkurrensmyndigheterna bör överväga att tillförordnainterimistiska åtgärder oftare, och att de kan förlita sig på den rättspraxis somfinns för att säkerställa att besluten kommer att motstå en överklagan.
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Boukhiar, Mohand-Akli. "Rôle du récepteur à l’antigène des cellules B (BCR) dans la survie des cellules du lymphome du manteau : Implication des facteurs de transcription STAT3 et EGR1." Paris 13, 2011. http://www.theses.fr/2011PA132045.
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Le lymphome à cellules du manteau (MCL) est un lymphome agressif caractérisé par une prolifération; de lymphocytes B matures CD5+ issus de la zone du manteau folliculaire des ganglions. Le MCL est défini pai' la translocation chromosomique t(11 ; 14) (q13 ; q32) qui entraine une surexpression de la cycline Dl. Cependant cette translocation ne suffit pas par elle-même pour induire la lymphomagénèse et des études récentes suggèrent un rôle de la sélection antigénique et de la signalisation du récepteur B (BCR) dans l'émergence du clone malin. Sur cette base, nous avons cherché à identifier dans des cellules primaires de patients MCL, des voies de signalisation dérégulées en aval du BCR et aboutissant à l'activation de facteurs de transcription impliqués dans les processus de survie des cellules tumorales. Nous avons tout d'abord montré que le facteur de transcription STAT3 est constitutivement phosphorylé dans les cellules de MCL et que cette phosphorylation est fortement augmentée en réponse à la stimulation du BCR. Les phosphorylations constitutive et induite par la stimulation du BCR de STAT3 sont le résultat d'une boucle autocrine de sécrétion d'IL6 et/ou d'IL10 dépendante du facteur de transcription NF-kB. L'inhibition de la voie Jak/STAT3 induit l'apoptose des cellules de MCL et supprime le signal de survie cellulaire induit par la stimulation antigénique. De plus, le traitement des cellules par le bortezomib, un inhibiteur du protéasome utilisé en clinique dans le traitement du MCL, supprime la phosphorylation de STAT3 ainsi que le signal de survie cellulaire induit par le BCR. Nous avons ensuite cherché à identifier d'autres facteurs de transcription, induits plus précocement en réponse à la stimulation du BCR et qui pourraient également être impliqués dans la dérégulation de la prolifération des cellules de MCL. Nous avons montré que la stimulation du BCR entraîne une augmentation importante et rapide (dès 30' avec maximum à 1h) du facteur de transcription EGR1 suivi de celle de c-MYC. De plus, l'inhibition spécifique de la kinase JNK constitutivement activée dans les cellules de MCL, entraîne une diminution de l'expression d'EGR1 associée à une augmentation de l'apoptose et à une inhibition du signal de survie cellulaire induit par le BCR. Par ailleurs, nous avons mis en évidence une activation constitutive des kinases de la famille Src (SFK) et plus précisément de Lyn, activation renforcée en réponse à la stimulation du BCR. Sur cette base, nous avons évalué l'efficacité du dasatinib (BMS-354825), une drogue qui cible les kinases SFK. Nous avons montré que le dasatinib à de très faibles doses (100nM) inhibe in vitro la phosphorylation constitutive et induite par le BCR de Lyn et de JNK, supprime l'expression d'EGR-1 et induit l'apoptose des cellules de patients leucémiques. En conclusion, nos résultats ont permis de mettre en évidence une dérégulation de voies de signalisation (SFK, JNK) et de facteurs de transcription (STAT3, EGR1, C-MYC) qui, de manière constitutive ou induite en réponse à la stimulation antigénique, participent au processus de prolifération et des cellules de MCL. L'ensemble de ces résultats ouvre ainsi la voie vers le développement de nouvelles stratégies thérapeutiques ciblées dans cette pathologieMantle cell lymphoma (MCL) is an aggressive and incurable malignant lymphoma, representing approximately 5% of non Hodgkin lymphomas. Its hallmark is the translocation t(11:14)q (13;32), leading to overexpression of cyclin Dl. However this chromosomal alteration is not sufficient to induce MCL and recent studies suggest the involvement of antigenic stimulation and B-cell receptor (BCR) signaling in this pathogenesis. In this context, we aimed at identifying in primary MCL cells deregulated signaling pathways downstream of BCR and leading to activation of transcription factors and to increased MCL cell survival. We evidenced a constitutive and BCR-induced phosphorylation of the transcription factor STAT3 resulting from an autocrine IL6 and/or IL10 secretion. Inhibition of the JAK/STAT3 pathway increased spontaneous apoptosis and suppressed BCR-induced cell survival. Moreover, treatment with Bortezomib induced apoptosis and a decrease of both IL6/IL10 secretions and STAT3 phosphorylation. In addition, bortezomib inhibited B-cell receptor-triggered STAT3 phosphorylation and cell survival. To further identify early genes involved in BCR-induced survival, we looked at differential expression of genes upon BCR stimulation and found that BCR engagement also led to a quick and transient induction of EGR1 expression, following by the one of c-Myc. We next evaluated the role of EGR1 in MCL cell survival and showed that inhibition of JNK by SP600125 induced a decrease of both constitutive and BCR-induced EGR1 expression, associated with an increase of apoptosis and a suppression of BCR-induced survival. We also showed that primary MCL cells displayed a constitutive and BCR-induced activation of Src family kinases including LYN and that efficient inhibition of these kinases by dasatinib led to apoptosis through inhibition of the downstream JNK/EGR1 pathway. In conclusion, our study performed on primary MCL lymphocytes evidenced that constitutive and BCRinduced signaling provide important survival signal which can be efficiently inhibited by Bortezomib and Dasatinib. Of interest, our result indicated for the first time that Dasatinib through inhibition of SFK/LYN kinases could be used as a new therapeutic agent in MCL by overcoming pro-survival signal emanating from the BCR
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Shi, Qiwen. "GADD45a-Targeted Suicide Gene Therapy for the Prevention or Treatment of Non-Small Cell Lung Carcinoma." Kent State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=kent1436485198.
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Marklund, Rikard, and Ricard Carlenius. "Sveriges och EG:s konkurrensrättsliga regler om gryningsräder i privata hem i förhållande till artikel 8 i Europakonventionen." Thesis, Örebro University, Department of Behavioural, Social and Legal Sciences, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-1610.
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Roitman, David. "Reform des EG-Wettbewerbsrechts die Gruppenfreistellungsverordnung für vertikale Vertriebsvereinbarungen und damit verbundene Aspekte der Verordnung 1, 2003." Hamburg Kovač, 2005. http://www.verlagdrkovac.de/3-8300-2204-2.htm.
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Roitman, David. "Reform des EG-Wettbewerbsrechts : Die Gruppenfreistellungsverordnung für vertikale Vertriebsvereinbarungen und damit verbundene Aspekte der Verordnung 1/ 2003 /." Hamburg : Kovač, 2006. http://www.verlagdrkovac.de/3-8300-2204-2.htm.
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Brunn, Thomas. "Die EG-Kartellverfahrensverordnung 1/2003 und ihre Auswirkungen auf die Gruppenfreistellungsverordnungen und die Entzugsverfahren der Vertikal-GVO /." Frankfurt am Main [u.a.] : Lang, 2004. http://www.gbv.de/dms/spk/sbb/recht/toc/387845151.pdf.
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Faria, Rulian Ricardo. "Sensibilidade diferencial aos efeitos comportamentais induzidos por etanol e sobre a expressão de c-Fos e Egr-1, entre camundongos adultos e adolescentes." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-04012008-160519/.
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A transição da adolescência (ADOLESC) para a idade adulta (ADULTO) é caracterizada por uma maturação de comportamentos, assim como de estruturas e sistemas do SNC. Este estudo investigou os efeitos da administração aguda e repetida de baixas doses de etanol (2,0 g/kg) em camundongos ADULTO (60 dias) e ADOLESC (28 dias), bem como a expressão de c-Fos e Egr-1 em distintas regiões cerebrais. Camundongos ADULTO e ADOLESC receberam agudamente salina (SAL) ou EtOH e sua atividade locomotora foi quantificada em campo aberto (CA). Uma hora após a injeção, a expressão de c-Fos e Egr-1 foi avaliada por imuno-histoquímica. Foram constatados: aumento na atividade locomotora e na expressão de c-Fos e Egr-1 nos animais tratados com EtOH. Outros animais ADULTO e ADOLESC foram tratados com EtOH ou SAL repetidamente (15 dias). Uma semana após o pré-tratamento, todos animais receberam etanol. A atividade locomotora foi quantificada e a expressão de c-Fos e Egr-1 foi avaliada. Os ADOLESC desenvolveram tolerância, enquanto que os ADULTO apresentaram sensibilização comportamental locomotora. A administração prolongada de etanol induziu alterações adaptativas diferenciadas, dependentes da idade, na expressão de c-Fos e Egr-1 em várias regiões encefálicas.The transition from adolescence (ADOLESC) into adulthood (ADULT) is characterized by behavioral maturation, as well as of structures and systems of CNS. This study investigated the behavioral effects of acute and repeated administration of EtOH (2,0 g/kg) in ADULT and ADOLESC mice, as well as the c-Fos and Egr-1 expression induced by EtOH in distinctive brain structures. Locomotor activity from ADULT and ADOLESC mice acutely treated with either saline (SAL) or EtOH was measured in open field (OF). One hour after injections, c-Fos and Egr-1 expressions were evaluated by immunohistochemistry. The results demonstrated increased locomotor activity and increased c-Fos and Egr-1 expression in EtOH-treated mice. Other groups of ADULT and ADOLESC mice were treated repeatedly with SAL or EtOH during 15 days. One week after this pretreatment, all animals received an injection of EtOH. The locomotor activity was quantified and c-Fos and Egr-1 expressions were evaluated. While ADULT mice presented behavioral sensitization, ADOLESC mice developed tolerance. The repeated administration of EtOH induced an age-dependent differential expression of c-Fos and Egr-1 in several brain regions.
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Arnold, Sylvia. "Der soziale Dialog nach Art. 139 EG eine Analyse unter besonderer Berücksichtigung der Legitimation des Ratsbeschlusses nach Art. 139 Abs. 2 S. 1 Alt. 2 EG." Baden-Baden Nomos, 2007. http://d-nb.info/987636022/04.
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Quinn, Jeffrey Alan. "Requirement of integrin [alpha]5[beta]1 and tyrosine phosphorylation of SHC for prohb-EGF release by GPR30, a seven transmembrane receptor for estrogen /." View online ; access limited to URI, 2006. http://0-wwwlib.umi.com.helin.uri.edu/dissertations/dlnow/3225328.
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Isele, Jan Felix. "Die Wettbewerbsverbote des 1 UWG im Lichte der Dienstleistungsfreiheit nach Artt. 49 ff. EGV : [eine Untersuchung der Gemeinschaftsrechtskonformität der großen Generalklausel des deutschen UWG] /." Frankfurt am Main [u.a.] : Lang, 2002. http://www.gbv.de/dms/spk/sbb/recht/toc/334720540.pdf.
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Saitzek, Sebastian. "Verpflichtungszusagen im europäischen Kartellrecht : nach Artikel 9 Verordnung (EG) Nr. 1/2003 des Rates vom 16. Dezember 2002 zur Durchführung der Artikel 81 und 82 des EG-Vertrages /." Hamburg : Kovač, 2008. http://www.verlagdrkovac.de/978-3-8300-3427-8.htm.
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