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Maxwell, Megan Amanda, i n/a. "PEX1 Mutations in Australasian Patients with Disorders of Peroxisome Biogenesis". Griffith University. School of Biomolecular and Biomedical Science, 2004. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20040219.100649.
Pełny tekst źródłaMaxwell, Megan Amanda. "PEX1 Mutations in Australasian Patients with Disorders of Peroxisome Biogenesis". Thesis, Griffith University, 2004. http://hdl.handle.net/10072/366184.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
Full Text
Stroobants, An Karin. "Studies on peroxisome biogenesis". [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2001. http://dare.uva.nl/document/60799.
Pełny tekst źródłaLi, Xiaoling. "Peroxisome proliferation and division". Available to US Hopkins community, 2002. http://wwwlib.umi.com/dissertations/dlnow/3080712.
Pełny tekst źródłaLiu, Xiaoxi. "BEYOND PEROXISOME: ABCD2 MODIFIES PPARα SIGNALING AND IDENTIFIES A SUBCLASS OF PEROXISOMES IN MOUSE ADIPOSE TISSUE". UKnowledge, 2014. http://uknowledge.uky.edu/pharmacy_etds/41.
Pełny tekst źródłaSadeghi, Azadi Afsoon. "Identification and characterization of novel signalling pathways involved in peroxisome proliferation in humans". Thesis, University of Exeter, 2018. http://hdl.handle.net/10871/33738.
Pełny tekst źródłaBell, Alexander. "The molecular basis of peroxisome proliferation". Thesis, University of Nottingham, 1998. http://eprints.nottingham.ac.uk/10395/.
Pełny tekst źródłaYaacob, Nik Soriani. "Molecular cell biology of peroxisome proliferators". Thesis, University of Surrey, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244831.
Pełny tekst źródłaCastro, Ines Gomes Oliveira. "Tail-anchored proteins at peroxisomes : identification of MIRO1 as a novel peroxisomal motility factor". Thesis, University of Exeter, 2016. http://hdl.handle.net/10871/24657.
Pełny tekst źródłaAnderson, Steven P. "Gene modulation during peroxisome proliferator-induced hepatocarcinogenesis". NCSU, 2001. http://www.lib.ncsu.edu/theses/available/etd-20011101-131940.
Pełny tekst źródłaANDERSON, STEVEN PAUL. Gene modulation in peroxisome proliferator-induced hepatocarcinogenesis. (Under the direction of Russell C. Cattley and John M. Cullen). Recognition that peroxisome proliferator chemicals are potent hepatic mitogens and carcinogens in rats and mice has generated concern about possible human health risks associated with exposure to several of these chemicals, many of which have medical or commercial utility. Our broad objective was to improve the estimation of human health risk following peroxisome proliferator exposure by defining a subset of the molecular events associated with the rodent tumors. Our working hypothesis was that peroxisome proliferator-induced tumors in rodents result from specific, peroxisome proliferator-activated receptor-a(Ppara)-modulated changes in gene expression. The research was directed toward three specific aims. First, we sought to identify genes associated with hepatocarcinogenesis induced by the peroxisome proliferator, Wy-14, 643, in the rat. The principle conclusion of these studies - that peroxisome proliferators dysregulate expression of hepatic acute-phase protein genes - suggested possible perturbations in cytokine signaling networks that also regulate cell growth. Second, although Ppara is necessary for the rodent hepatocarcinogenesis induced by peroxisome proliferators, we were interested in identifying more proximate mediators of the increased cell proliferation. Thus, we examined cytokine signaling in mice treated with peroxisome proliferators. We found that peroxisome proliferator-induced increases in cell proliferation is not mediated via Tnfasignaling, but instead may be mediated through interleukin-1b or interleukin-6. Third, because Ppara is necessary for the cell proliferation that follows peroxisome proliferator exposure, we hypothesized that the receptor may play a role in hepatocellular proliferation induced by other stimuli. Following partial hepatectomy, liver regeneration in Ppara-null mice is transiently impaired, and may result from altered expression of genes regulating the G1/S cell cycle checkpoint in hepatocytes from these mice. Overall, our studies suggest that hepatic Ppara activation (1) alters inflammatory mediators, (2) modulates several potentially mitogenic cytokines, and (3) is necessary for normal liver regeneration after partial hepatectomy. Our data, compared with data from similar experiments on human hepatocytes, may provide further clues about the differences and similarities between peroxisome proliferator exposure in humans and laboratory animals.
Nwosu, V. U. "Peroxisome enzymes in animal models of obesity". Thesis, University of Wolverhampton, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.380662.
Pełny tekst źródłaMitchell, Angela M. "Hepatic peroxisome proliferation : mechanisms and species differences". Thesis, University of Surrey, 1985. http://epubs.surrey.ac.uk/847808/.
Pełny tekst źródłaNickkho-Amiry, Mahshid. "Peroxisome proliferator-activated receptors in endometrial cancer". Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/peroxisome-proliferatoractivated-receptors-in-endometrial-cancer(2388ac43-ecd4-402f-a9c7-853be4902ec8).html.
Pełny tekst źródłaHarper, Courtney Christine. "Complex problems in peroxisome matrix protein import". Available to US Hopkins community, 2003. http://wwwlib.umi.com/dissertations/dlnow/3080674.
Pełny tekst źródłaTinfo, Nicole Shivonn. "The peroxisome proliferator-activated receptor in ovarian biology". [Ames, Iowa : Iowa State University], 2007.
Znajdź pełny tekst źródłaAl, Kholaifi Abdullah. "The induction of liver growth by peroxisome proliferators". Thesis, University of Nottingham, 2008. http://eprints.nottingham.ac.uk/10443/.
Pełny tekst źródłaBrowne, P. O. "Analyses of the peroxisome proliferator-activated receptor gamma". Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597020.
Pełny tekst źródłaDionisi, Mauro. "Endocannabinoid metabolism and peroxisome proliferator-activated receptor signalling". Thesis, University of Nottingham, 2010. http://eprints.nottingham.ac.uk/11384/.
Pełny tekst źródłaFerreira, Joana Filipa Dias. "The role of STING on peroxisome-dependent signalling". Master's thesis, Universidade de Aveiro, 2017. http://hdl.handle.net/10773/21999.
Pełny tekst źródłaViruses are recognized by several cellular sensors from the innate immune system, activating signalling cascades which result in the production of interferons and other cytokines that affect the virus life cycle and hinder spreading to other cells. Although the RIG-I/MAVS and the STING pathways are assumed to signal, respectively, for RNA and DNA viruses, there is still some controversy on how these pathways interact with and influence each other. The interaction between STING and MAVS, previously reported to take place at mitochondria, supports a crosslink between these pathways. Our group has recently demonstrated that STING is also able to interact with the peroxisomal MAVS. With this work we aimed at studying in more detail the interplay between the STING pathway and the peroxisomal RIG-I/MAVS pathway. One of our approaches involved the knock-down of STING and stimulation of the RIGI/ MAVS pathway in cells that contained MAVS solely at peroxisomes, in order to study the importance of STING for the establishment of an effective peroxisome-dependent antiviral response. In parallel, we activated STING by transfecting 2’3’-cGAMP with the objective of performing RT-qPCR analysis of the peroxisome-dependent production of cytokines. The studies initiated with this thesis will contribute to the unravelling of the interplay between the STING pathways and the peroxisomal-dependent RIG-I/MAVS signalling.
Os vírus são reconhecidos por vários sensores do sistema imunitário inato, responsáveis pela ativação de cascatas de sinalização que levam à produção de interferões e citoquinas, impedindo o ciclo viral e a propagação da infeção às células vizinhas. Apesar de a via da RIG-I/MAVS e da STING serem respetivamente responsáveis pelo reconhecimento de vírus de ARN e ADN, existe ainda alguma controvérsia sobre como estas duas vias interagem. A interação entre a STING e a MAVS, anteriormente reportada nas mitocôndrias, sugere uma interligação entre as duas vias. O nosso grupo demonstrou recentemente que existe também uma interação entre a STING e a MAVS peroxisomal. Neste trabalho, o nosso objetivo consistiu em estudar a interligação entre a via da STING e a via RIG-I/MAVS peroxisomal. Começamos por silenciar a STING e a estimular a via RIG-I/MAVS numa linha celular que contem MAVS apenas nos peroxissomas, para estudar a influência da STING na resposta antiviral dependente dos peroxissomas. Por outro lado, tentamos ativar a STING através da transfeção da molécula 2’3’-cGAMP com o objetivo de analisar a produção de citoquinas e interferões dependentes da via peroxissomal por RT-qPCR. As experiências apresentadas nesta tese irão certamente contribuir para desvendar a interligação entre a via da STING e a via RIG-I/MAVS dependente dos peroxissomas.
Heß, Katharina Andrea. "Peroxisome proliferator-activated receptors (PPARs) und die Lymphozytenmigration". [S.l. : s.n.], 2006. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-56139.
Pełny tekst źródłaAl, Saryi Nadal. "Molecular studies of peroxisome biogenesis in Saccharomyces cerevisiae". Thesis, University of Sheffield, 2016. http://etheses.whiterose.ac.uk/13433/.
Pełny tekst źródłaMarcus, Sandra L. "Transcriptional regulation of rat peroxisomal acyl-CoA oxidase and enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase by peroxisome proliferators". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ34808.pdf.
Pełny tekst źródłaAnderson, I. W. "Permeability of leaf peroxisomes to photorespiratory metabolites". Thesis, University of Oxford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379882.
Pełny tekst źródłaMakowska, Janet Mary. "Species differences in the hepatic and renal responses to ciprofibrate". Thesis, University of Surrey, 1988. http://epubs.surrey.ac.uk/847765/.
Pełny tekst źródłaMehl, Isaac R. "Regulation of gene expression by peroxisome proliferator activated receptors". 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?p3249923.
Pełny tekst źródłaTitle from first page of PDF file (viewed April 4, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
Gootjes, Jeannette. "Molecular, biochemical and clinical aspects of peroxisome biogenesis disorders". [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2004. http://dare.uva.nl/document/74957.
Pełny tekst źródłaMontgomery, S. "The biochemistry and ultrastructure of glyoxysome and peroxisome development". Thesis, University of Oxford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376933.
Pełny tekst źródłaOwens, Joanna. "Regulation of peroxisome proliferator-activated receptor-alpha (PPAR#alpha#)". Thesis, University of Surrey, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341337.
Pełny tekst źródłaChoudhury, Munim. "PPARalpha in peroxisome proliferation : molecular characterisation and species differences". Thesis, University of Nottingham, 2000. http://eprints.nottingham.ac.uk/10396/.
Pełny tekst źródłaSavory, Richard. "PPAR#alpha# : inducibility and species differences in expression". Thesis, University of Nottingham, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337248.
Pełny tekst źródłaXie, Weiqiao Hope Lila W. "Isolation and characterization of a gene required for peroxisome biogenesis". Oregon Health & Science University, 1993. http://content.ohsu.edu/u?/etd,234.
Pełny tekst źródłaMolecular Biology
This thesis describes the cloning and analysis of PER6, a gene required for peroxisome biogenesis in Pichia pastoris. The gene was cloned by functional complementation of a per6 P. pastoris mutant strain that was one of a number of peroxisome-deficient mutants isolated in this laboratory. The complementing activity was localized to a small DNA fragment by subcloning and Northern filter hybridization analysis and the DNA sequence of the fragment was determined. The sequence revealed a 1296-bp open reading frame which potentially encodes a 432-amino acid protein of 49 kD. The gene was transcribed into a message of 1.4 kilobases that was constitutively expressed but induced several-fold in cells growing on methanol. A mutant strain with a deletion of a large portion of the open reading frame was constructed and used to genetically demonstrate that the cloned gene was identical to the defective gene in the originally isolated per6 mutant. The predicted amino acid sequence of the PER6 product revealed several interesting features, including a significant regional similarity to PAF-1, a gene known to be defective in some patients with Zellweger syndrome, a lethal human genetic disease caused by peroxisome deficiency. Finally, the PER6 product was produced in E. coli and purified to serve as antigen for antibody production.
Xie, Weiqiao. "Isolation and characterization of a gene required for peroxisome biogenesis /". Full text open access at:, 1993. http://content.ohsu.edu/u?/etd,234.
Pełny tekst źródłaBrown, Trevor Wayne. "A study of peroxisome biogenesis in the yeast Yarrowia lipolytica". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0014/MQ60095.pdf.
Pełny tekst źródłaAmer, Abeer H. A. "Mechanism of action of liver growth induced by peroxisome proliferators". Thesis, University of Nottingham, 2011. http://eprints.nottingham.ac.uk/11947/.
Pełny tekst źródłaDe, Mora Kim Stephen. "Foundational technologies in synthetic biology : promoter measurement and peroxisome engineering". Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/7870.
Pełny tekst źródłaKaplan, Claude Paul. "Isolation and characterisation of genes involved in plant peroxisome biogenesis". Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627157.
Pełny tekst źródłaNguyen, Tam Hong. "Pex13 Mutant Mice as Models for the Peroxisome Biogenesis Disorders". Thesis, Griffith University, 2008. http://hdl.handle.net/10072/366797.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Physical Sciences
Science, Environment, Engineering and Technology
Full Text
Smith, Steven Andrew. "The role of Peroxisome proliferator-activated receptors in the rat brain /". St. Lucia, Qld, 2004. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17982.pdf.
Pełny tekst źródłaRoberts, Lee D. "Defining the metabolic effect of peroxisome proliferator-activated receptor δ activation". Thesis, University of Cambridge, 2010. https://www.repository.cam.ac.uk/handle/1810/226743.
Pełny tekst źródłaEitzen, Gary A. "An analysis of peroxisome assembly mutants of the yeast Yarrowia lipolytica". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq22978.pdf.
Pełny tekst źródłaLagali, Pamela Sarita. "Studies of peroxisome proliferator-activated receptors in transcriptional processes and disease". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ34386.pdf.
Pełny tekst źródłaCheng, Wai. "The relationship between peroxisome proliferator-activated receptors (PPARs) and cell proliferation /". View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36433937.
Pełny tekst źródłaLuense, Lacey Jeanne. "The role of peroxisome proliferator activated-receptor gamma in ovarian function". [Ames, Iowa : Iowa State University], 2007.
Znajdź pełny tekst źródłaHughes, Robert Ian. "The role of peroxisome proliferator activated receptor agonists in Cardiovascular disease". Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.504931.
Pełny tekst źródłaCheng, Wai, i 鄭蔚. "The relationship between peroxisome proliferator-activated receptors (PPARs) and cell proliferation". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B45010614.
Pełny tekst źródłaShiau, Chung-Wai. "Thiazolidinediones: from peroxisome-proliferator-activated receptor γ(PPARγ) to anticancer agents". The Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=osu1128111032.
Pełny tekst źródłaWei, Shuo. "Peroxisome Proliferator-Activated Receptor γ (PPARγ)-Independent Antitumor Effect of Thiazolidinediones". The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1259167390.
Pełny tekst źródłaBrown, Emily Lauren. "Regulation of Peroxisome Proliferator-Activated Receptor Alpha by Selected Beta-Apocarotenoids". The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1275401911.
Pełny tekst źródłaRangwala, Shamina M. "In vitro mechanistic studies of peroxisome proliferation by chiral clofibrate analogs /". The Ohio State University, 1997. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487946776024538.
Pełny tekst źródłaPinho, Sónia Andreia de Almeida. "Induction and determination of ROS and their effect on peroxisome dynamics". Master's thesis, Universidade de Aveiro, 2010. http://hdl.handle.net/10773/3160.
Pełny tekst źródłaPeroxissomas são organelos celulares de membrana simples, os quais têm importantes funções metabólicas, como por exemplo metabolismo de lípidos e ROS, sendo assim indispensáveis para a saúde e desenvolvimento humano. Os peroxissomas são organelos altamente flexíveis e dinâmicos que rapidamente se agregam, multiplicam e degradam em resposta a necessidades metabólicas. Em cultura celular, o stress oxidativo e outros estímulos externos (ex. factores de crescimento, ácidos gordos, despolimerização) têm mostrado induzir processos de crescimento (alongamento) e divisão de peroxissomas, os quais estão relacionados com a sua proliferação. Considerando que alguns dos componentes moleculares da maquinaria de crescimento e divisão têm sido identificados nos últimos anos, as vias de sinalização e regulação que medeiam a proliferação de peroxissomas são largamente desconhecidas. O objectivo desta dissertação de mestrado foi examinar o efeito de diferentes estímulos externos promotores de ROS na indução do crescimento/proliferação do compartimento peroxisomal. Foi seleccionado um sistema de cultura de células de mamífero que apresentam um compartimento peroxisomal dinâmico. Análises baseadas em fluorescência para a detecção da produção de ROS e alterações nos níveis de GSH intracelular foram estabelecidos. Estes procedimentos foram usados primeiro para esclarecer se o alongamento de peroxissomas observado após despolimerização de microtubulos (pelo nocodazole) é mediado por ROS. O alongamento de peroxissomas e a despolimerização dos microtubulos após tratamento com nocodazole foi monitorizado e quantificado por microscopia de imunofluorescência. O Nocodazole induziu um aumento dos níveis de ROS intracelular e apesar do pré tratamento com antioxidantes ter baixado os níveis de ROS, não preveniu o alongamento peroxisomal. Estes resultados demonstram que as alterações morfológicas do compartimento peroxisomal induzidas pelo nocodazole são independentes da produção de ROS. Para além disso, foi examinado o efeito de alterações nos níveis de glutationa (GSH) celular no compartimento peroxisomal. Interessantemente, a redução dos níveis de GSH intracelular pelo BSO, um inibidor da enzima γ-glutamylcystein synthetase (γ-GCS), resultou num aumento acentuado de crescimento/proliferação de peroxissomas. Os níveis de ROS e GSH foram determinados por análises baseadas em fluorescência. Pré tratamento com antioxidante preveniu o alongamento de peroxissomas indicando que a alteração no estado redox celular (citoplasmatico) levou à proliferação de peroxissomas a qual exerce, supostamente, uma função protectora para a célula. Finalmente, foi investigado se a inibição da cadeia respiratória mitocondrial e com isso, se ROS provenientes das mitocondrias foi capaz de induzir crescimento e divisão dos peroxissomas. Entre os inibidores analisados, apenas a rotenona, inibidor do complexo I, teve um efeito proeminente na elongação de peroxissomas. Todavia, foi demontrado que o seu efeito é devido à acção que a rotenona tem na despolimerização dos microtubulos. Assim, apesar da relação de proximidade entre mitocondria e peroxissomas, as ROS provenientes das mitocondrias não são prováveis de induzir alterações no compartimento peroxisomal. Os nossos resultados também indicam que estudos in vivo usando a rotenona têm de ser interpretados com muito cuidado. Além disso, os resultados mostram que as ROS podem alterar a dinâmica do compartimento peroxissomal, mas têm de vir de locais específicos dentro da célula (por exemplo, do citosol). ABSTRACT: Peroxisomes are single membrane bound subcellular organelles, which fulfill important metabolic functions, for example in lipid and ROS metabolism, and are thus indispensable for human health and development. Peroxisomes are highly flexible organelles that rapidly assemble, multiply and degrade in response to metabolic needs. In cultured cells, oxidative stress and other external stimuli (e. g. growth factors, fatty acids, microtubule depolymerization) have been shown to induce processes of growth (elongation) and division of peroxisomes, which are related to peroxisome proliferation. Whereas some of the molecular components of the growth and division machinery have been identified in the last years, the regulatory and signaling pathways mediating peroxisome proliferation are largely unknown. The aim of this master thesis was to examine the effects of different ROS-producing external stimuli on the induction of growth/proliferation of the peroxisomal compartment. A suitable mammalian cell culture system with a dynamic peroxisomal compartment was selected and fluorescent-based assays for the detection of ROS production and changes in the intracellular GSH levels were established. The setup was first used to clarify if peroxisome elongation observed after depolymerization of microtubules (by nocodazole) is mediated by ROS. Peroxisome elongation and microtubule depolymerization after nocodazole treatment was monitored and quantified by immunofluorescence microscopy. Although nocodazole induced an increase in cellular ROS levels, a pre-treatment with antioxidants and lowering of intracellular ROS levels did not prevent peroxisome elongation. These findings demonstrate that the morphological changes of the peroxisomal compartment induced by nocodazole are independent of ROS production. Furthermore, I examined the effect of changes in the cellular redox state on the peroxisomal compartment. Interestingly, the reduction of intracellular GSH levels by BSO, an inhibitor of γ- glutamylcystein synthetase (γ-GCS), resulted in a prominent increase in peroxisomal growth/elongation. ROS and GSH levels were determined by fluorescent-based assays. Pre-treatment with antioxidants prevented peroxisome elongation indicating that changes in the cellular (cytoplasmic) redox state lead to peroxisome proliferation, which is supposed to have a protective function for the cell. Finally, I investigated whether inhibition of the mitochondrial respiratory chain and thus, mitochondriaderived ROS were capable of inducing peroxisomal growth and division. Among the inhibitors tested, only rotenone, a complex I inhibitor, had a prominent effect on peroxisome elongation. However, I demonstrated that this effect is due to a microtubule-depolymerizing activity of rotenone. Thus, despite the close peroxisomemitochondria relationship, mitochondria-derived ROS are unlikely to induce changes of the peroxisomal compartment. Our findings also indicate that in vivo studies using rotenone have to be interpreted with great care. In addition, the results show that ROS can alter the dynamics of the peroxisomal compartment, but have to come from specific locations (e.g. the cytosol) within the cell.