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1
Karnati, Srikanth. "Functional characterization of peroxisomes and pathological consequences of peroxisomal dysfunction in the lung." Giessen : VVB Lauferweiler, 2009. http://d-nb.info/100020572X/04.
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Castro, 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.
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Peroxisomes are dynamic and multifunctional organelles, which are essential for human health and development. They are remarkably diverse, with functions that vary significantly between cells and organisms, and can dramatically change their size, shape and dynamics in response to cellular cues. In the past few years, several studies have significantly increased our understanding of the basic principles that enable peroxisome biogenesis and degradation, as well as their pivotal role in cellular signalling and homeostasis. However, several of these processes are still poorly understood. In this thesis we initially studied the peroxisome targeting mechanism of a group of C-terminally anchored membrane proteins, known as tail-anchored (TA) proteins. In order to investigate the molecular signals that enable TA protein targeting to cellular organelles, we analysed the physicochemical properties of a cohort of TA proteins both in silico and in vivo, and show that a combination of transmembrane domain (TMD) hydrophobicity and C-terminal tail charge determines organelle-specific targeting. Focusing on peroxisomes, we demonstrate that a balance between TMD hydrophobicity and high positive tail charge directs TA proteins to this organelle, and enables binding to the peroxisomal chaperone PEX19. These results allowed us to create a bioinformatical tool to predict the targeting of uncharacterised TA proteins and further develop our understanding of the molecular mechanisms involved in the targeting of this protein group. From our initial TA protein screen, we identified the TA protein MIRO1 at peroxisomes and looked at its role in the regulation of peroxisome motility. We show that endogenous MIRO1 localises to mitochondria and peroxisomes, and that dual targeting depends on the C-terminal tail. MIRO1 expression significantly increased peroxisome motility in several cell lines, and revealed a role for motility in peroxisome dynamics, by inducing organelle proliferation and elongation. These results reveal a new molecular complex at peroxisomes and provide us with a tool to further dissect the role of motility on peroxisome function.
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Liu, 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.
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ABCD2 (D2) has been proposed as a peroxisomal long-chain acyl-CoA transporter that is essential for very long chain fatty acid metabolism. In the livers of mice, D2 is highly induced by fenofibrate, a PPARα ligand that has been widely used as a lipid lowering agent in the treatment of hypertriglyceridemia. To determine if D2 is a modifier of fibrate responses, wild-type and D2 deficient mice were treated with fenofibrate for 14 days. The absence of D2 altered expression of gene clusters associated with lipid metabolism, including PPARα signaling. Using 3T3-L1 adipocytes, which express high levels of D2, we confirmed that knock-down of D2 modified genomic responses to fibrate treatment. We next evaluated the impact of D2 on effects of fibrates in a mouse model of dietinduced obesity. Fenofibrate treatment opposed the development of obesity, hypertriglyceridemia, and insulin resistance. However, these effects were unaffected by D2 genotype. We concluded that D2 can modulate genomic responses to fibrates, but that these effects are not sufficiently robust to alter the effects of fibrates on diet-induced obesity phenotypes.
Although proposed as a peroxisomal transporter, the intracellular localization of D2, especially in adipose tissue, has not been validated with direct experimental evidence. Sequential centrifugation of mouse adipose homogenates generated a fraction enriched with D2, but lacked well-known peroxisome markers including catalase, PEX19, and ABCD3 (D3). Electron microscopic imaging of this fraction confirmed the presence of D2 protein on an organelle with evidence of a dense matrix and a diameter of ~200 nm, the typical structure and size of a microperoxisome. D2 and PEX19 antibodies recognized distinct structures in mouse adipose. Immunoisolation of the D2-containing compartment from adipose tissue confirmed the scarcity of PEX19. Proteomic profiling of the D2 compartment revealed the presence of proteins associated peroxisome, endoplasmic reticulum (ER), and mitochondria. We conclude that D2 is localized to a distinct subclass of peroxisomes that lack many peroxisome proteins and may physically associate with mitochondria and the ER.
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Aboushadi, Nahla Mohamed. "Role of peroxisomes in isoprenoid biosynthesis /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2000. http://wwwlib.umi.com/cr/ucsd/fullcit?p9963646.
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Karnati, Srikanth [Verfasser]. "Functional characterization of peroxisomes and pathological consequences of peroxisomal dysfunction in the lung / by Srikanth Karnati." Giessen : VVB Laufersweiler, 2009. http://d-nb.info/999686674/34.
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Bottger, Gina. "Receptor-mediated import of proteins into peroxisomes." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2001. http://dare.uva.nl/document/60502.
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Vries, Bart de. "The biology of peroxisomes in Hansenula polymorpha." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2008. http://irs.ub.rug.nl/ppn.
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Anderson, 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.
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Drago, Ilaria. "Ca2+ homeostasis in mammalian and plant peroxisomes." Doctoral thesis, Università degli studi di Padova, 2009. http://hdl.handle.net/11577/3426033.
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Peroxisomes are single-membrane bound organelles involved in reactive oxygen species scavenging, ?- and ?-oxidation of fatty acids, biosynthesis of ether phospholipids and other metabolic pathways. Although recent studies have highlighted the mechanisms of peroxisomal formation, fusion-fission, protein import etc. little information is available concerning a possible role of peroxisomes in cellular signalling, and, until very recently, no information was available about a possible role of peroxisomes in cellular Ca2+ handling. Ca2+ signalling exerts a plethora of functions in cells (both in physiology and pathology) and while the role of subcellular compartments like endoplasmic reticulum, mitochondria, nucleus and Golgi apparatus in Ca2+ handling has been intensively investigated in the last decades, peroxisomes remained a black whole in the picture. Last, but not least, a renewed interest towards peroxisome functions has been triggered by the discovery of a number of human diseases (called “peroxisomal disorders”) that are due to mutations of peroxisomal proteins. For all these reasons, I decided to investigate if and how peroxisomes play a role in cellular Ca2+ handling. I targeted a genetically encoded, FRET-based Ca2+ sensor to peroxisomal matrix and I found that the Ca2+ concentration of peroxisomes in living cells at rest is similar to that of the cytosol, while increases in cytosolic Ca2+ concentration (elicited by either Ca2+ mobilization from stores or Ca2+ influx through plasma membrane Ca2+ channels) are usually followed by a slow rise in intraperoxisomal Ca2+ concentration. I also investigated the mechanism of peroxisomal Ca2+ entry and I found that Ca2+ influx into peroxisomes is not driven by an ATP-dependent pump, membrane potential or H+ (Na+) gradients. However, the peroxisomal membrane appears to play a low-pass filter role, preventing the organelle from taking up Ca2+ during short lasting cytosolic Ca2+ transients, while allowing equilibration of the peroxisomal luminal Ca2+ concentration with that of the cytosol during prolonged cytosolic Ca2+ increases. Thus, peroxisomes appear to be an additional cytosolic Ca2+ buffer, but their influx and efflux mechanisms are unlike those of any other cellular organelle. The second part of my work was aimed at understanding the physiological function of this phenomenon. To date, no Ca2+-regulated mammalian peroxisomal enzyme is known. On the contrary, there are some Ca2+-regulated plant peroxisomal enzymes, in particular an isoform of the H2O2 scavenging enzyme catalase, Cat3. Cat3 has been shown to be specifically located in plant peroxisomes and to be activated in vitro by Ca2+ and calmodulin. The peroxisomal Ca2+ probe employed in the first part of this work was expressed in plant peroxisomes and revealed that the phenomenon of Ca2+ entry into peroxisomal matrix in plants is very similar, both in amplitude and kinetic, to that of mammalian cells. Plasma membrane hyperpolarization demonstrated to be a reliable stimulus to trigger a prolonged rise of peroxisomal (and cytosolic) Ca2+ concentration and so it was chosen in order to verify if a peroxisomal Ca2+ rise can somehow affect H2O2 scavenging. Preliminary experiments performed in Arabidopsis plants stably expressing in peroxisomes a H2O2 sensor indicate that H2O2 scavenging is accelerated by Ca2+ entry and this is correlated with the level of Cat3 within peroxisomes.I perossisomi sono degli organelli intracellulari circondati da una singola membrana coinvolti nell’eliminazione di specie reattive dell’ossigeno, ?- e ?-ossidazione di acidi grassi, biosintesi di eteri di fosfolipidi e in altre reazioni metaboliche. Sebbene studi recenti abbiano elucidato i meccanismi alla base della formazione, della fusione- fissione e dell’importo di proteine nella matrice dei perossisomi, le informazioni riguardanti il ruolo dei perossisomi nel signalling cellulare sono scarse e, fino a poco tempo fa, quelle riguardanti il possibile ruolo dei perossisomi nel signalling cellulare del Ca2+ erano totalmente assenti. Il signalling del Ca2+ è alla base di un ampio numero di funzioni cellulari sia fisiologiche che patologiche e mentre il ruolo di compartimenti subcellulari come il reticolo endoplasmico, i mitocondri, il nucleo e l’apparato di Golgi nelle dinamiche intracellulari del Ca2+ è stato ampiamente studiato negli ultimi decenni, i perossisomi sono rimasti nella “zona d’ombra” di questo scenario. Infine, c’è stato ultimamente un rinnovato interesse circa le funzioni dei perossisomi grazie alla scoperta di un certo numero di malattie umane (chiamate “disordini dei perossisomi”) dovute a mutazioni di proteine perossisomiali. Per tutte queste ragioni, ho deciso di investigare se, e come, i perossisomi rivestono un qualche ruolo nell’omeostasi intracellulare del Ca2+. A questo scopo ho indirizzato alla matrice dei perossisomi una sonda per il Ca2+ geneticamente codificata e basata su FRET e ho potuto dimostrare che la concentrazione di Ca2+ nei perossisomi di cellule vive in condizioni di riposo è molto simile a quella citosolica mentre aumenti della concentrazione di Ca2+ (causati sia da mobilizzazione di Ca2+ dai depositi intracellulari che da influsso attraverso canali per il Ca2+ situati nella membrana plasmatica) sono solitamente seguiti da un lento aumento della concentrazione di Ca2+ nella matrice perossisomiale. Mi sono inoltre occupata della caratterizzazione del meccanismo che sta alla base dell’entrata di Ca2+ nei perossisomi e sono arrivata alla conclusione che questo fenomeno non è dovuto alla presenza di una pompa dipendente da ATP, né di un potenziale di membrana o di un gradiente di H+ o Na+. La membrana dei perossisomi sembra costituire una barriera che previene l’entrata di Ca2+ nel caso di aumenti brevi nel tempo, mentre nel caso di aumenti prolungati della concentrazione di Ca2+ nel citosol permette una lenta equilibrazione della concentrazione di Ca2+ nella matrice perossisomiale con l’ambiente citosolico. I perossisomi sembrano quindi costituire un nuovo sistema-tampone per il Ca2+del citosol, sebbene il loro meccanismo di influsso ed efflusso per il Ca2+ è totalmente differente da quello di ogni altro organello cellulare. La seconda parte del mio lavoro si è poi concentrata sullo studio dei possibili ruoli fisiologici del fenomeno dell’entrata di Ca2+ nei perossisomi. In letteratura non sono al momento riportati degli enzimi localizzati nei perossisomi delle cellule di mammifero che siano regolati da Ca2+; al contrario, alcuni enzimi localizzati nei perossisomi delle piante sembrano essere regolati da Ca2+. Di questi, quello che più mi è sembrato interessante è un’isoforma di un enzima deputato all’eliminazione di H2O2, la catalasi. L’attività di Cat3 è infatti riportata essere attivata in vitro da Ca2+ e calmodulina. La sonda per il Ca2+ utilizzata per lo studio dei perossisomi in cellule di mammifero è stata quindi indirizzata ai perossisomi di cellule vegetali e ha permesso di dimostrare che il fenomeno dell’entrata di Ca2+ nei perossisomi è molto simile, sia per ampiezza che per cinetica, tra perossisomi di mammifero e di pianta. L’iperpolarizzazione della membrana plasmatica ha dimostrato essere uno stimolo ripetibile che causa un prolungato aumento della concentrazione di Ca2+ nei perossisomi (e nel citosol) di pianta ed è quindi stato scelto per verificare se un aumento di Ca2+ nei perossisomi possa in qualche modo influenzare l’eliminazione di H2O2. Esperimenti preliminari effettuati in piante di Arabidopsis che esprimono stabilmente una sonda per H2O2 geneticamente codificata indicano che l’eliminazione di H2O2 è notevolmente accelerata in seguito all’entrata di Ca2+; questo correla con il livello di Cat3 espressa nei perossisomi.
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Smith, Jennifer Joy. "Maintenance of peroxisomes 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_0008/NQ59670.pdf.
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Tappia, Paramjit Singh. "Analysis of peroxisomes from mammalian intestine and liver." Thesis, University of Wolverhampton, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306242.
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Guedes, Mariana da Rocha Soares. "Mitochondria and peroxisomes : role within cellular antiviral defense." Master's thesis, Universidade de Aveiro, 2014. http://hdl.handle.net/10773/12960.
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Mestrado em Biomedicina MolecularThe present paper presents a review and compilation of all the scientifically relevant bibliography to date, regarding the antiviral signalling pathways implicated in the cellular innate immune system in humans. Emphasizing the mitochondrial antiviral signalling adaptor (MAVS), this paper explores the special features of the signal transduction pathways and their components in two specific organelles: mitochondria and peroxisomes. These pathways, ultimately, result in the expression of interferon-stimulated genes (ISGs), which are primarily responsible for fighting against viral replication, viral particle assembly and virion release within the cell. In this paper, several proposals for further investigation are also presented, since there is still a lot to learn about the role of peroxisomes in the antiviral innate immune responses.
O presente trabalho propõe-se a rever e compilar toda a bibliografia cientificamente relevante até à data, no que respeita as vias de sinalização antivirais implicadas na imunidade celular inata em células humanas. Com ênfase na proteína adaptadora MAVS, este trabalho explora as particularidades das vias de transdução de sinal e respetivos intervenientes em dois organelos celulares específicos: mitocôndrias e peroxissomas. Estas vias, em última instância, resultam na expressão de genes estimulados por interferões (ISGs), principais responsáveis pelo combate celular eficaz contra a replicação viral, montagem de partículas virais e libertação de viriões na célula infetada. Neste trabalho são ainda apresentadas propostas para investigações futuras, uma vez que ainda muito pouco se sabe sobre o papel dos peroxissomas nas respostas imunitárias inatas contra infeções virais.
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Parshyna, Iryna. "Autophagic degradation of peroxisomes in the alkane-assimilating yeast Yarrowia lipolytica." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2006. http://nbn-resolving.de/urn:nbn:de:swb:14-1164836301920-35300.
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The thesis is aimed at understanding of molecular mechanisms of autophagic degradation of peroxisomes (pexophagy) in the yeast Yarrowia lipolytica. This microorganism has been extensively used to explore peroxisome biogenesis (Titorenko and Rachubinski, 2000). Gunkel et al. (1999) intoduced Y. lypolitica into pexophagy studies. However, the field of pexophagic research on this yeast remains quite unexplored. This work involved following tasks: (1) the development and optimization of Y. lipolytica as a model system to study peroxisome degradation; (2) Y. lipolytica genes and proteins implicated in pexophagy should be found and characterized; (3) a proper easy-to-handle selection procedure to isolate novel peroxisome degradation-deficient(pdd) mutants of Y. lipolytica should be devised.
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Xie, 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.
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M.S.Molecular 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.
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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.
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Klein, André Theodoor Jan. "Pex5p, a guide for import of proteins into peroxisomes." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2003. http://dare.uva.nl/document/69923.
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Boateng, Eistine [Verfasser]. "The Role of Peroxisomes in Pulmonary Fibrosis / Eistine Boateng." Gießen : Universitätsbibliothek, 2019. http://d-nb.info/1199264539/34.
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Alves, Sandra Manuela Carvalho. "Exploring the role of peroxisomes in Helicobacter pylori infection." Master's thesis, Universidade de Aveiro, 2015. http://hdl.handle.net/10773/14216.
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Mestrado em Biomedicina MolecularThe Helicobacter pylori is a gram-negative microaerophilic bacterium. Humans are the principal reservoir and it has been estimated that about 50% of the world population is infected by this bacterium, even though only about 20% of the patients present symptoms. The H. pylori colonizes the human gastric mucosa and is associated to several gastrointestinal diseases, such chronic gastritis, peptic ulceration and gastric cancer. Peroxisomes are membrane-enclosed subcellular organelles, which can be virtually found in all eukaryotic cells. They are involved in several metabolic reactions, with emphasis for the fatty acid oxidation, lipid biosynthesis and hydrogen peroxide detoxification. It is increasingly accepted that peroxisomes are more than simple metabolic organelles within cells. Previous studies of viral infections have demonstrated that peroxisomes are involved in the cellular innate immune response. It has also been suggested that all bacterial and viral pathogens may be exposed to peroxisomal recognition. Thus, it becomes important to better study the role of the peroxisomes in response to infections. In the present work we have analysed the possible peroxisomal alterations in morphology, number and enzymatic function in infected cells with the main aim of exploring a possible role for peroxisomes in H. pylori infection. The obtained results suggest that H. pylori infection does not affect significantly the peroxisomal morphology, number or localization. However, the results obtained suggested that H. pylori infection affects the amount of peroxisomal catalase, probably due to an increase of ROS in the cellular environment, as a consequence of the bacterial infection.
Helicobacter pylori é uma bactéria gram-negativa microaerofílica. Os seres humanos são o seu principal reservatório e estima-se que cerca de 50% da população mundial encontra-se infetada, embora apenas cerca de 20% dos pacientes apresentem sintomas. H. pylori coloniza a mucosa gástrica humana e está associada a várias doenças gastrointestinais, como gastrite crónica, úlcera péptica e cancro gástrico. Os peroxissomas são organelos de membrana simples, que se encontram virtualmente em todas as células eucarióticas. Nestes ocorrem várias reações metabólicas, com destaque para a oxidação dos ácidos gordos, a biossíntese de lípidos e a desintoxicação do peróxido de hidrogénio. É cada vez mais aceite que os peroxissomas desempenham muito mais do que simples funções metabólicas. Em estudos anteriores foi demonstrado que os peroxissomas estão envolvidos na resposta imune em infeções virais. Para além disso, foi sugerido que tanto os patogénios bacterianos como os virais podem ser expostos ao reconhecimento peroxissomal. Assim, torna-se importante estudar melhor o papel dos peroxissomas em resposta a infeções. No presente trabalho foram analisadas possíveis alterações peroxisomais relativamente à sua morfologia, número e função enzimática, em células infetadas, com o principal objetivo de explorar o possível papel dos peroxissomas na infeção por H. pylori. Os resultados obtidos sugerem que a infeção por H. pylori não afeta significativamente a morfologia, número ou localização dos peroxissomas. No entanto, os resultados sugerem que a infeção por H. pylori afeta a quantidade de catalase peroxissomal, provavelmente devido a um aumento das EROs no meio celular, resultante da infeção bacteriana.
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Maxwell, Megan Amanda, and 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.
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The peroxisome is a subcellular organelle that carries out a diverse range of metabolic functions, including the b-oxidation of very long chain fatty acids, the breakdown of peroxide and the a-oxidation of fatty acids. Disruption of peroxisome metabolic functions leads to severe disease in humans. These diseases can be broadly grouped into two categories: those in which a single enzyme is defective, and those known as the peroxisome biogenesis disorders (PBDs), which result from a generalised failure to import peroxisomal matrix proteins (and consequently result in disruption of multiple metabolic pathways). The PBDs result from mutations in PEX genes, which encode protein products called peroxins, required for the normal biogenesis of the peroxisome. PEX1 encodes an AAA ATPase that is essential for peroxisome biogenesis, and mutations in PEX1 are the most common cause of PBDs worldwide. This study focused on the identification of mutations in PEX1 in an Australasian cohort of PBD patients, and the impact of these mutations on PEX1 function. As a result of the studies presented in this thesis, twelve mutations in PEX1 were identified in the Australasian cohort of patients. The identified mutations can be broadly grouped into three categories: missense mutations, mutations directly introducing a premature termination codon (PTC) and mutations that interrupt the reading frame of PEX1. The missense mutations that were identified were R798G, G843D, I989T and R998Q; all of these mutations affect amino acid residues located in the AAA domains of the PEX1 protein. Two mutations that directly introduce PTCs into the PEX1 transcript (R790X and R998X), and four frameshift mutations (A302fs, I370fs, I700fs and S797fs) were identified. There was also one mutation found in an intronic region (IVS22-19A>G) that is presumed to affect splicing of the PEX1 mRNA. Three of these mutations, G843D, I700fs and G973fs, were found at high frequency in this patient cohort. At the commencement of these studies, it was hypothesised that missense mutations would result in attenuation of PEX1 function, but mutations that introduced PTCs, either directly or indirectly, would have a deleterious effect on PEX1 function. Mutations introducing PTCs are thought to cause mRNA to be degraded by the nonsense-mediated decay of mRNA (NMD) pathway, and thus result in a decrease in PEX1 protein levels. The studies on the cellular impact of the identified PEX1 mutations were consistent with these hypotheses. Missense mutations were found to reduce peroxisomal protein import and PEX1 protein levels, but a residual level of function remained. PTC-generating mutations were found to have a major impact on PEX1 function, with PEX1 mRNA and protein levels being drastically reduced, and peroxisomal protein import capability abolished. Patients with two missense mutations showed the least impact on PEX1 function, patients with two PTC-generating mutations had a severe defect in PEX1 function, and patients carrying a combination of a missense mutation and a PTC-generating mutation showed levels of PEX1 function that were intermediate between these extremes. Thus, a correlation between PEX1 genotype and phenotype was defined for the Australasian cohort of patients investigated in these studies. For a number of patients, mutations in the coding sequence of one PEX1 allele could not be identified. Analysis of the 5' UTR of this gene was therefore pursued for potential novel mutations. The initial analyses demonstrated that the 5' end of PEX1 extended further than previously reported. Two co-segregating polymorphisms were also identified, termed 137 T>C and 53C>G. The -137T>C polymorphism resided in an upstream, in-frame ATG (termed ATG1), and the possibility that the additional sequence represented PEX1 coding sequence was examined. While both ATGs were found to be functional by virtue of in vitro and in vivo expression investigations, Western blot analysis of the PEX1 protein in patient and control cell extracts indicated that physiological translation of PEX1 was from the second ATG only. Using a luciferase reporter approach, the additional sequence was found to exhibit promoter activity. When examined alone the -137T>C polymorphism exerted a detrimental effect on PEX1 promoter activity, reducing activity to half that of wild-type levels, and the -53C>G polymorphism increased PEX1 promoter activity by 25%. When co-expressed (mimicking the physiological condition) these polymorphisms compensated for each other to bring PEX1 promoter activity to near wild-type levels. The PEX1 mutations identified in this study have been utilised by collaborators at the National Referral Laboratory for Lysosomal, Peroxisomal and Related Genetic Disorders (based at the Women's and Children's Hospital, Adelaide), in prenatal diagnosis of the PBDs. In addition, the identification of three common mutations in Australasian PBD patients has led to the implementation of screening for these mutations in newly referred patients, often enabling a precise diagnosis of a PBD to be made. Finally, the strong correlation between genotype and phenotype for the patient cohort investigated as part of these studies has generated a basis for the assessment of newly identified mutations in PEX1.
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Maxwell, Megan Amanda. "PEX1 Mutations in Australasian Patients with Disorders of Peroxisome Biogenesis." Thesis, Griffith University, 2004. http://hdl.handle.net/10072/366184.
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The peroxisome is a subcellular organelle that carries out a diverse range of metabolic functions, including the b-oxidation of very long chain fatty acids, the breakdown of peroxide and the a-oxidation of fatty acids. Disruption of peroxisome metabolic functions leads to severe disease in humans. These diseases can be broadly grouped into two categories: those in which a single enzyme is defective, and those known as the peroxisome biogenesis disorders (PBDs), which result from a generalised failure to import peroxisomal matrix proteins (and consequently result in disruption of multiple metabolic pathways). The PBDs result from mutations in PEX genes, which encode protein products called peroxins, required for the normal biogenesis of the peroxisome. PEX1 encodes an AAA ATPase that is essential for peroxisome biogenesis, and mutations in PEX1 are the most common cause of PBDs worldwide. This study focused on the identification of mutations in PEX1 in an Australasian cohort of PBD patients, and the impact of these mutations on PEX1 function. As a result of the studies presented in this thesis, twelve mutations in PEX1 were identified in the Australasian cohort of patients. The identified mutations can be broadly grouped into three categories: missense mutations, mutations directly introducing a premature termination codon (PTC) and mutations that interrupt the reading frame of PEX1. The missense mutations that were identified were R798G, G843D, I989T and R998Q; all of these mutations affect amino acid residues located in the AAA domains of the PEX1 protein. Two mutations that directly introduce PTCs into the PEX1 transcript (R790X and R998X), and four frameshift mutations (A302fs, I370fs, I700fs and S797fs) were identified. There was also one mutation found in an intronic region (IVS22-19A>G) that is presumed to affect splicing of the PEX1 mRNA. Three of these mutations, G843D, I700fs and G973fs, were found at high frequency in this patient cohort. At the commencement of these studies, it was hypothesised that missense mutations would result in attenuation of PEX1 function, but mutations that introduced PTCs, either directly or indirectly, would have a deleterious effect on PEX1 function. Mutations introducing PTCs are thought to cause mRNA to be degraded by the nonsense-mediated decay of mRNA (NMD) pathway, and thus result in a decrease in PEX1 protein levels. The studies on the cellular impact of the identified PEX1 mutations were consistent with these hypotheses. Missense mutations were found to reduce peroxisomal protein import and PEX1 protein levels, but a residual level of function remained. PTC-generating mutations were found to have a major impact on PEX1 function, with PEX1 mRNA and protein levels being drastically reduced, and peroxisomal protein import capability abolished. Patients with two missense mutations showed the least impact on PEX1 function, patients with two PTC-generating mutations had a severe defect in PEX1 function, and patients carrying a combination of a missense mutation and a PTC-generating mutation showed levels of PEX1 function that were intermediate between these extremes. Thus, a correlation between PEX1 genotype and phenotype was defined for the Australasian cohort of patients investigated in these studies. For a number of patients, mutations in the coding sequence of one PEX1 allele could not be identified. Analysis of the 5' UTR of this gene was therefore pursued for potential novel mutations. The initial analyses demonstrated that the 5' end of PEX1 extended further than previously reported. Two co-segregating polymorphisms were also identified, termed –137 T>C and –53C>G. The -137T>C polymorphism resided in an upstream, in-frame ATG (termed ATG1), and the possibility that the additional sequence represented PEX1 coding sequence was examined. While both ATGs were found to be functional by virtue of in vitro and in vivo expression investigations, Western blot analysis of the PEX1 protein in patient and control cell extracts indicated that physiological translation of PEX1 was from the second ATG only. Using a luciferase reporter approach, the additional sequence was found to exhibit promoter activity. When examined alone the -137T>C polymorphism exerted a detrimental effect on PEX1 promoter activity, reducing activity to half that of wild-type levels, and the -53C>G polymorphism increased PEX1 promoter activity by 25%. When co-expressed (mimicking the physiological condition) these polymorphisms compensated for each other to bring PEX1 promoter activity to near wild-type levels. The PEX1 mutations identified in this study have been utilised by collaborators at the National Referral Laboratory for Lysosomal, Peroxisomal and Related Genetic Disorders (based at the Women's and Children's Hospital, Adelaide), in prenatal diagnosis of the PBDs. In addition, the identification of three common mutations in Australasian PBD patients has led to the implementation of screening for these mutations in newly referred patients, often enabling a precise diagnosis of a PBD to be made. Finally, the strong correlation between genotype and phenotype for the patient cohort investigated as part of these studies has generated a basis for the assessment of newly identified mutations in PEX1.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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Ferreira, Ana Rita Filgueiras. "Hepatitis C virus and peroxisomes : evasion from the cellular antiviral response." Master's thesis, Universidade de Aveiro, 2015. http://hdl.handle.net/10773/14348.
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Mestrado em Biomedicina MolecularHepatitis C virus (HCV) causes the most prevalent viral infection worldwide. Upon infection, the HCV genome is detected by the RIG-I-MAVS signalling pathway leading to the production of direct antiviral effectors. NS3/4A protease is the main inhibitor of innate immunity against HCV and it was found to inhibit the mitochondrial signalling protein (MAVS). MAVS was recently found to localize at peroxisomes coordinating with mitochondria the activation of effective antiviral response. Peroxisomal MAVS is responsible for inducing a rapid but short termed antiviral response that is IFNindependent, contrary to mitochondrial MAVS which is associated with the activation of an IFN-dependent antiviral response with delayed kinetics. With this work we aimed at evaluating the effect of NS3/4A over the peroxisomal– MAVS pathway. Our results showed that the MAVS localizing exclusively at peroxisomes is targeted by the HCV NS3/4A protease. We also show that the MAVS cleavage by NS3/4A impaired the antiviral response mediated by peroxisomal-MAVS. These results reaffirm the importance of peroxisomes for viral-host interaction and in antiviral defences. Further studies are proposed in order to better understand the role of this organelle in innate immunity. These may lead to the improvement of therapy against HCV infection.
O vírus da hepatite C (VHC) provoca a infeção viral mais prevalente em todo o mundo. Após infeção, o genoma do VHC é detetado pela via de sinalização RIGI- MAVS levando à produção de efetores diretos da resposta antiviral. A protease NS3/4A é o principal inibidor da resposta imune produzido pelo VHC e foi descrito como inibidor da proteína MAVS. A proteína MAVS foi recentemente localizada nos peroxissomas que, juntamente com a mitocôndria, coordenam a resposta antiviral. A MAVS peroxisomal é responsável pela indução de uma resposta antiviral rápida mas de curta duração que é independente de interferões, mas pelo contrário, a MAVS mitocondrial está associada a uma ativação da resposta antiviral que é dependente de interferões mas que se caracteriza por uma cinética retardada. O nosso objetivo com este trabalho consistiu em avaliar o efeito da NS3/4A na via de sinalização coordenada pelos peroxissomas. Os nossos resultados mostram que a MAVS localizada nos peroxissomas é alvo da protease NS3/4A do VHC. Também mostramos que a clivagem da proteína MAVS pela NS3/4A inibe a resposta antiviral mediada pela MAVS peroxissomal. Estes resultados reafirmam a importância dos peroxissomas na interação vírushospedeiro e na defesa antiviral. Futuros estudos são aconselhados para que se compreenda a função dos peroxissomas na imunidade inata. Estes podem levar a uma melhoria na terapia da infeção pelo VHC.
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Zwacka, Ralf Michael. "The human homologue of the murine glomerulosclerosis gene Mpv17." Thesis, Open University, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262628.
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Munck, Joanne Marie. "Molecular characterisation of the maintenance of peroxisomes in saccharoyces cerevisiae." Thesis, University of Sheffield, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.489055.
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Eukaryotic cells use a range of mechanisms to ensure that a full complement of each organelle is maintained during cell division. In S.cerevisiae cells, the maintenance of peroxisomes requires the growth, division and accurate segregation of existing peroxisomes. Alternatively, peroxisomes can be formed de novo from the ER. However, this process only occurs when the inheritance of peroxisomes is abolished.
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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.
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Fan, Wei [Verfasser]. "The role of peroxisomes in osteoblast differentiation and functions / Wei Fan." Gießen : Universitätsbibliothek, 2015. http://d-nb.info/1077170742/34.
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Soliman, Kareem [Verfasser], Jutta [Akademischer Betreuer] Gärtner, Silvio [Gutachter] Rizzoli, and Stefan [Gutachter] Jakobs. "Characterization of peroxisomes and peroxisome deficient cell lines by super-resolution microscopy and biochemical methods / Kareem Soliman ; Gutachter: Silvio Rizzoli, Stefan Jakobs ; Betreuer: Jutta Gärtner." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2016. http://d-nb.info/1140641921/34.
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El-Merhie, Natalia [Verfasser]. "The role of peroxisomes in chronic obstructive pulmonary disease / Natalia El-Merhie." Gießen : Universitätsbibliothek, 2017. http://d-nb.info/1147680590/34.
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Fredericks, Ernst. "Molecular signaling in colorectal carcinogenesis : the roles and relationships of beta-catenin, PPARgamma and COX-2." Thesis, Nelson Mandela Metropolitan University, 2013. http://hdl.handle.net/10948/d1021014.
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Colorectal cancer (CRC) is a common disease with significant morbidity and mortality. In spite of significant advances in understanding the molecular signaling in this disorder, unanswered questions remain. Cyclooxygenase-2 (COX-2) and β-catenin have established roles in colorectal carcinogenesis, with both being upregulated early in the disease course. The role of peroxisome proliferator-activated receptor γ (PPARγ) is less clear, but has been shown to be downregulated in colon cancer models. Butyrate, a short chain fatty acid, produced by colon microbiota and transported into the colonocyte by transporter proteins, appears to be important in early carcinogenesis. The butyrate concentration is reduced in CRC and so are its transporters. Interleukin-17 (IL-17) plays a role in colitis-associated colorectal cancer (CAC), but its function in sporadic CRC is less clear. Similarly, Protein kinase C (PKC) has proven involvement in many solid tumours, including CRC, but its exact mechanistic role is still speculative. AIM: To investigate the role and possible signaling pathways of the major role players, β-catenin, COX-2 and PPARγ in early CRC. Further, to elucidate the mechanistic pathways of butyrate and its transporters, IL-17 and PKC in CRC. METHOD: Informed consent was obtained for all patients. Patients were recruited in various disease categories, including normal, irritable bowel syndrome (IBS), inflammatory bowel disease (IBD) and CRC. Colon biopsy specimens were obtained during colonoscopy and used for immunohistochemistry (IHC) and gene expression analysis of the above genes by quantitative polymerase chain reaction (qPCR). RESULTS: β-catenin mRNA and protein expression was increased in CRC and the IBD groups compared to the normal group, while it was reduced in the IBS groups. COX-2 mRNA expression showed a steady increase from normal, through IBS, IBD and CRC groups to a statistically significant degree. The COX-2 protein expression, however, did not match the mRNA expression with increased COX-2 protein expression in normal and IBS groups and reduced expression in IBD and CRC groups. PPARγ mRNA expression was unchanged in IBD and CRC groups, but significantly increased in the IBS group compared to normal. Butyrate transporter, SLC16A1 mRNA was significantly reduced in CRC, but also in the IBS groups, which was unexpected. In the IBD group, SLC16A1 mRNA was unchanged in Crohn’s disease (CD) but significantly reduced in ulcerative colitis (UC). Similarly, SLC5A8 mRNA expression was significantly reduced in the CRC as well as the IBS groups. In the IBD groups, SLC5A8 was unchanged in UC but significantly increased in CD. IL-17 mRNA expression was significantly reduced in CRC and IBS groups, but unchanged in the IBD groups. PKCε mRNA was significantly increased in CRC as expected. In the IBD groups, PKCε mRNA was unchanged in CD but significantly increased in UC. In the IBS groups, PKCε mRNA in constipation –IBS (C-IBS) was significantly reduced, but unchanged in diarrhoea – IBS (D-IBS). CONCLUSIONS: β-catenin mRNA and protein expression was increased in CRC and the CRC promoting IBD groups. COX-2 protein expression was incongruent with the COX-2 mRNA expression and this may reflect homeostatic control mechanisms. High COX-2 mRNA expression in CRC and CRC promoting IBD groups may be a secondary phenomenon reflecting the inflammatory milieu, rather than a true carcinogenesis-related event. PPARγ does not appear to play a central role in early colon carcinogenesis, in spite of available literature suggesting otherwise. Butyrate transporters showed inconsistent results and for now no firm conclusions can be drawn from this. IL-17 may play a role in CAC as confirmed in this and other studies, but its role in sporadic CRC is tenuous and requires further investigation. Likewise for PKCε, upregulation is associated with increased tumourigenecity as shown in this study, however, the mechanistic pathway(s) involved is still speculative and requires further study.
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De, Mora Kim Stephen. "Foundational technologies in synthetic biology : promoter measurement and peroxisome engineering." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/7870.
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The confluence of next generation DNA sequencing and synthesis when combined with the application of concepts such as standardization and modular design has led to the genesis of a new discipline. The nascent field of Synthetic Biology concerns the rational design and construction of genetic circuits, pathways, machines and eventually whole organisms. The immaturity of this field dictates that early research efforts, including this Thesis, describe foundational work towards the creation of tools which make biology more amenable to being engineered. The first part of this Thesis describes an attempt to standardize the measurement of transcriptional promoter activity in E. coli. A method to measure in vivo promoter activity was developed for E. coli and tested in a multi-institution trial. Comparable results were achieved with less than a two-fold range for the measured promoters across eight laboratories. A standardized measurement kit was created and distributed for use by the teams participating in the 2008 international Genetically Engineered Machines competition. Techniques learned measuring the activity of E. coli promoters were applied to a collection of S. cerevisiae strains. Several promoters were measured in synthetic dextrose media and ADH1 was measured in multiple media conditions. The outcome of these experiments is to consider proposing ADH1as the reference promoter in S. cerevisiae. The second aspect of this Thesis describes the construction of artificial organelles in S. cerevisiae. Artificial organelles hold the prospect of being able to insulate synthetic genetic pathways from the cell. Two proteins are essential for the biogenesis of the peroxisome organelle in humans and yeast, Pex3p and Pex19p. Pex3p functions as a peroxisomal membrane receptor for Pex19p, while Pex19p shuttles other peroxisomal proteins to the membrane, including Pex3p, creating a feedback loop. Human Pex19p has previously been shown to dock to yeast Pex3p and a version of yeast Pex19p has been shown to work with human Pex3p as a high degree of evolutionary conservation exists between these proteins. Because of these inter-species protein docking characteristics, there exists the possibility of creating bimodality: the ambition of the work was therefore to create a cell strain which possessed both synthetic “humanized” and natural yeast peroxisomes. An S. cerevisiae BY4741a derivative strain was engineered with fluorophore tagged versions of human (CFP) and yeast (YFP) Pex3p and untagged yeast and human Pex19p proteins. The results indicated the creation of a single population of peroxisomes when a measure of fluorescently imaged CFP and YFP peroxisomes were plotted on a scatter plot. A log of the ratio of CFP to YFP peroxisomes was plotted on a histogram and a normal distribution was found to best fit the curve, indicating a lack of bimodality. Finally, microscopy images of this strain were reviewed and by visual inspection, showed no evidence of distinct human or yeast peroxisomes. This experiment therefore produced no evidence of bimodality when examining the interactions of human and yeast Pex3p and Pex19p proteins. However, the four proteins were shown to interact closely to produce a single population of chimeric human-yeast peroxisomes. The peroxisome-deficient mutant phonotype strain was rescued using human Pex3p and Pex19p.
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Johnson, Monique A. "Novel genetic selections for peroxisome biogenesis mutants (pex) and the isolation and characterization of PEX14 and Pex14p in Pichia Pastoris /." Full text open access at:, 2000. http://content.ohsu.edu/u?/etd,15.
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Ozeki, Katharine. "Pichia pastoris Rppa09976 is a peroxisomal membrane-associated ACBP domain-containing protein, delivered to peroxisomes from the ER, and is required for their selective degradation." Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p1465084.
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Thesis (M.S.)--University of California, San Diego, 2009.Title from first page of PDF file (viewed June 19, 2009). Available via ProQuest Digital Dissertations. Includes bibliographical references.
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Delille, Hannah Katharina [Verfasser], and Ralf [Akademischer Betreuer] Jacob. "Biogenesis of peroxisomes in mammalian cells : Characterization of the Pex11 proteins and their role in peroxisomal growth and division / Hannah Katharina Delille. Betreuer: Ralf Jacob." Marburg : Philipps-Universität Marburg, 2011. http://d-nb.info/1013075285/34.
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Logan, Heather Elizabeth. "Phosphatidylcholine turnover and protein kinase C in human fibroblasts with mutations affecting peroxisomes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/mq24866.pdf.
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Wood, Adrian J. "Subcellular analysis of normal and pathological gastrointestinal tissue with specific reference to peroxisomes." Thesis, University of Wolverhampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386569.
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Resende, Albina Dolores Cardoso da Silva Castro. "Seasonal and toxicological study of brown trout (Salmo trutta) kidney and liver peroxisomes." Doctoral thesis, Instituto de Ciências Biomédicas Abel Salazar, 2008. http://hdl.handle.net/10216/7260.
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Resende, Albina Dolores Cardoso da Silva Castro. "Seasonal and toxicological study of brown trout (Salmo trutta) kidney and liver peroxisomes." Tese, Instituto de Ciências Biomédicas Abel Salazar, 2008. http://hdl.handle.net/10216/7260.
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Chakraborty, Anirban [Verfasser], Ralf [Gutachter] Erdmann, and Christian [Gutachter] Herrmann. "New insights into de novo biogenesis of peroxisomes and into peroxisome proliferation in accharomyces cerevisiae / Anirban Chakraborty ; Gutachter: Ralf Erdmann, Christian Herrmann ; Fakultät für Chemie und Biochemie." Bochum : Ruhr-Universität Bochum, 2018. http://d-nb.info/1191481360/34.
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Chauhan, Dushyant. "Protein import into peroxisomes and oxidative stress: a study to elucidate the potential functional role of the conserved cysteine in Pex5p." Thesis, Högskolan i Skövde, Institutionen för vård och natur, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-5888.
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The oxidation status of a cell plays a crucial role in aging. As cells get aged, their redox state gets increased. Pex5p is a peroxisomal recycling receptor which binds to newly synthesized cargo proteins in the cytosol and imports them across the peroxisomal membrane. During this transport event, Pex5p gets monoubiquitinated at a conserved cysteine (C11) residue. This C11 is very essential for the recycling of Pex5p from the peroxisomal membrane to back into the cytosol. If the cysteine is replaced by serine, Pex5p does not get recycled back to the cytosol and accumulates on the peroxisomal membrane. In the present study, we have investigated whether the C11 in Pex5p could act as a redox switch. We measured the redox state of the cytosol and the peroxisomal matrix as well as the subcellular localization of catalase in aging cells. We found that an increase in the redox state of peroxisomes (in WT) leads to an increase in the redox state of the cytosol, which ultimately results in the impairment of PTS1 import. Interestingly, in the C11K condition, we did not see an impairment of PTS1 import. These observations support our hypothesis that C11 may act as a redox switch. We also performed some challenging experiments with H2O2. The results of these experiments show that a) import of catalase into peroxisomes sensitizes the cytosol and b) catalase overexpression does have a protective effect against oxidative stress caused by H2O2. In summary the results of our experiments support our hypothesis. However, further evaluation is needed to reveal the precise role of C11 in Pex5p function during cellular aging.
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Miyata, Kenji Sean. "The molecular mechanism of transcriptional activation by the peroxisome proliferator activated-receptor (alpha) /." *McMaster only, 1999.
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Guo, Guanlun. "Stereo-selective binding of enantiomeric ligands in PPAR[gamma] : a molecular modeling study." HKBU Institutional Repository, 2013. http://repository.hkbu.edu.hk/etd_ra/1516.
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Babujee, Lavanya. "Proteome studies on leaf peroxisomes from Spinacia oleracea L. and Arabidopsis thaliana (L.) Heynh." Doctoral thesis, [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972079734.
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Vasko, Radovan [Verfasser], Hassan [Akademischer Betreuer] Dihazi, and Michael [Akademischer Betreuer] Thumm. "Peroxisomes and Kidney Damage / Radovan Vasko. Gutachter: Hassan Dihazi ; Michael Thumm. Betreuer: Hassan Dihazi." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2014. http://d-nb.info/1064404030/34.
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Bonilla-Martinez, Hermelinda del Rocio [Verfasser]. "Peroxisomes in endocrine pancreatic islets, possible protectors against lipotoxicity? / Hermelinda del Rocio Bonilla-Martinez." Gießen : Universitätsbibliothek, 2019. http://d-nb.info/1185976922/34.
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Alkuwayti, Mayyadah. "The role of peroxisomes in sterol biosynthesis by the cellular slime mould Dictyostelium discoideum." Thesis, University of Sheffield, 2014. http://etheses.whiterose.ac.uk/7085/.
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In eukaryotic cells, the mevalonate pathway of isoprenoid biosynthesis provides the cell with essential precursors for several cellular processes. For example, one product, FDP (farnesyl diphosphate) is a fundamental precursor for sterol biosynthesis and it is also used for protein prenylation. In the slime mould Dictyostelium discoideum some of the mevalonate pathway enzymes possess a peroxisomal targeting signal. This suggested that part of the mevalonate pathway may take place in the peroxisomes. In this study, the intracellular locations of the mevalonate pathway enzymes were investigated by transforming D. discoideum amoebae to express each enzyme as a fusion protein with either GFP (green fluorescent protein) or mRFP (monomeric red fluorescent protein). It was found that three of the mevalonate pathway enzymes are peroxisomal: 3-hydroxy-3-methylglutaryl-coenzyme A synthase isozyme B, phosphomevalonate kinase and farnesyl diphosphate synthase. HMG-CoA reductase is associated with the endoplasmic reticulum and the other four enzymes of the mevalonate pathway were most likely to be in the cytosol: HMG-CoA synthase isozyme A, mevalonate kinase, diphosphomevalonate decarboxylase and IDP-isomerase. The intracellular location of the first five enzymes involved in sterol biosynthesis from farnesyl diphosphate was also identified by using the GFP or mRFP tagged enzyme approach. Some of these enzymes possess a strong peroxisomal targeting signal type 1 (PTS1). It was shown that the first four enzymes of the pathway: squalene synthase, squalene epoxidase, oxidosqualene cyclase and cycloartenol -C-24-methyltransferase are peroxisomal whereas the two isozymes of the fifth enzyme, methylsterol monooxygenase, are associated with the endoplasmic reticulum. It was also demonstrated that the first four enzymes on the sterol biosynthesis pathway are strongly associated with the peroxisomal membrane. However, the putative PTS1 present at the C-terminus of squalene synthase, oxidosqualene cyclase and cycloartenol-C-24-methyltransferase would imply that each of these enzymes should be a peroxisomal matrix protein. We therefore investigated whether the putative PTS1s are involved in directing these three enzymes into the peroxisomes. It was found that squalene synthase was largely peroxisomal even when its PTS1 was absent but the PTS1 in oxidosqualene synthase and cycloartenol-C-24-methyltransferase was essential for entry of these enzymes into peroxisomes. It appears that the sterol biosynthesis in D. discoideum is unusual since the enzymes squalene synthase, squalene epoxidase, oxidosqualene cyclase and cycloartenol-C-24-methyltransferase are accumulated in the peroxisomes whereas in all other organisms studied they are in the endoplasmic reticulum.
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Nenicu, Anca [Verfasser]. "Influence of peroxisomes on development, maturation and adult functions of the testis / Anca Nenicu." Giessen : VVB Laufersweiler, 2010. http://d-nb.info/1008505536/34.
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Cheng, 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.
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Westin, Maria A. K. "Acyl-CoA thioesterases - auxiliary enzymes in peroxisomal lipid metabolism /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-241-5/.
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Ching, Steven LK. "Arabidopsis glyoxylate reductase 1 is localized in the cytosol and not peroxisomes in plant cells." Thesis, Journal of Intergrative Plant Biology, 2012. http://hdl.handle.net/10214/3330.
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Glyoxylate reductase (GLYR) is a key enzyme in plant metabolism which catalyzes the detoxification of both photorespiratory glyoxylate and succinic semialdehdye, an intermediate of the γ-aminobutyrate (GABA) pathway. Two isoforms of GLYR exist in plants, GLYR1 and GLYR2, and while GLYR2 is known to be localized in plastids, GLYR1 has been reported to be localized in either peroxisomes or the cytosol. Here, the intracellular localization of Arabidopsis GLYR1 was reappraised by conducting microscopy-based experiments that address some novel mechanisms by which proteins can be directed to peroxisomes. For instance, the C-terminal tripeptide sequence of GLYR1, -SRE, despite its resemblance to a type 1 peroxisomal targeting signal, was not sufficient for peroxisomal targeting. Collectively, the results define the cytosol as the intracellular location of GLYR1 and provide a useful reference for future studies of proteins proposed to be localized to peroxisomes and/or the cytosol.NSERC
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Behari, Richa. "Establishment and characterisation of an in vitro system for import of proteins into plant peroxisomes." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283921.
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Wang, Yunhong [Verfasser], and Christian [Akademischer Betreuer] Schultz. "Subcellular distributions of peroxisomes and endoplasmic reticulum in hippocampal neurons / Yunhong Wang ; Betreuer: Christian Schultz." Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://d-nb.info/1185170901/34.
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