Relevant bibliographies by topics / PEX1

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'PEX1'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "PEX1"

1

Knoops, Kèvin, Rinse de Boer, Anita Kram, and Ida J. van der Klei. "Yeast pex1 cells contain peroxisomal ghosts that import matrix proteins upon reintroduction of Pex1." Journal of Cell Biology 211, no. 5 (December 7, 2015): 955–62. http://dx.doi.org/10.1083/jcb.201506059.

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Pex1 and Pex6 are two AAA-ATPases that play a crucial role in peroxisome biogenesis. We have characterized the ultrastructure of the Saccharomyces cerevisiae peroxisome-deficient mutants pex1 and pex6 by various high-resolution electron microscopy techniques. We observed that the cells contained peroxisomal membrane remnants, which in ultrathin cross sections generally appeared as double membrane rings. Electron tomography revealed that these structures consisted of one continuous membrane, representing an empty, flattened vesicle, which folds into a cup shape. Immunocytochemistry revealed that these structures lack peroxisomal matrix proteins but are the sole sites of the major peroxisomal membrane proteins Pex2, Pex10, Pex11, Pex13, and Pex14. Upon reintroduction of Pex1 in Pex1-deficient cells, these peroxisomal membrane remnants (ghosts) rapidly incorporated peroxisomal matrix proteins and developed into peroxisomes. Our data support earlier views that Pex1 and Pex6 play a role in peroxisomal matrix protein import.
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2

Verner, Zdeněk, Vojtěch Žárský, Tien Le, Ravi Kumar Narayanasamy, Petr Rada, Daniel Rozbeský, Abhijith Makki, et al. "Anaerobic peroxisomes in Entamoeba histolytica metabolize myo-inositol." PLOS Pathogens 17, no. 11 (November 15, 2021): e1010041. http://dx.doi.org/10.1371/journal.ppat.1010041.

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Entamoeba histolytica is believed to be devoid of peroxisomes, like most anaerobic protists. In this work, we provided the first evidence that peroxisomes are present in E. histolytica, although only seven proteins responsible for peroxisome biogenesis (peroxins) were identified (Pex1, Pex6, Pex5, Pex11, Pex14, Pex16, and Pex19). Targeting matrix proteins to peroxisomes is reduced to the PTS1-dependent pathway mediated via the soluble Pex5 receptor, while the PTS2 receptor Pex7 is absent. Immunofluorescence microscopy showed that peroxisomal markers (Pex5, Pex14, Pex16, Pex19) are present in vesicles distinct from mitosomes, the endoplasmic reticulum, and the endosome/phagosome system, except Pex11, which has dual localization in peroxisomes and mitosomes. Immunoelectron microscopy revealed that Pex14 localized to vesicles of approximately 90–100 nm in diameter. Proteomic analyses of affinity-purified peroxisomes and in silico PTS1 predictions provided datasets of 655 and 56 peroxisomal candidates, respectively; however, only six proteins were shared by both datasets, including myo-inositol dehydrogenase (myo-IDH). Peroxisomal NAD-dependent myo-IDH appeared to be a dimeric enzyme with high affinity to myo-inositol (Km 0.044 mM) and can utilize also scyllo-inositol, D-glucose and D-xylose as substrates. Phylogenetic analyses revealed that orthologs of myo-IDH with PTS1 are present in E. dispar, E. nutalli and E. moshkovskii but not in E. invadens, and form a monophyletic clade of mostly peroxisomal orthologs with free-living Mastigamoeba balamuthi and Pelomyxa schiedti. The presence of peroxisomes in E. histolytica and other archamoebae breaks the paradigm of peroxisome absence in anaerobes and provides a new potential target for the development of antiparasitic drugs.
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Agrawal, Gaurav, Scott N. Fassas, Zhi-Jie Xia, and Suresh Subramani. "Distinct requirements for intra-ER sorting and budding of peroxisomal membrane proteins from the ER." Journal of Cell Biology 212, no. 3 (February 1, 2016): 335–48. http://dx.doi.org/10.1083/jcb.201506141.

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During de novo peroxisome biogenesis, importomer complex proteins sort via two preperoxisomal vesicles (ppVs). However, the sorting mechanisms segregating peroxisomal membrane proteins to the preperoxisomal endoplasmic reticulum (pER) and into ppVs are unknown. We report novel roles for Pex3 and Pex19 in intra–endoplasmic reticulum (ER) sorting and budding of the RING-domain peroxins (Pex2, Pex10, and Pex12). Pex19 bridged the interaction at the ER between Pex3 and RING-domain proteins, resulting in a ternary complex that was critical for the intra-ER sorting and subsequent budding of the RING-domain peroxins. Although the docking subcomplex proteins (Pex13, Pex14, and Pex17) also required Pex19 for budding from the ER, they sorted to the pER independently of Pex3 and Pex19 and were spatially segregated from the RING-domain proteins. We also discovered a unique role for Pex3 in sorting Pex10 and Pex12, but with the docking subcomplex. Our study describes an intra-ER sorting process that regulates segregation, packaging, and budding of peroxisomal importomer subcomplexes, thereby preventing their premature assembly at the ER.
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4

Miyata, Non, and Yukio Fujiki. "Shuttling Mechanism of Peroxisome Targeting Signal Type 1 Receptor Pex5: ATP-Independent Import and ATP-Dependent Export." Molecular and Cellular Biology 25, no. 24 (December 15, 2005): 10822–32. http://dx.doi.org/10.1128/mcb.25.24.10822-10832.2005.

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ABSTRACT Peroxisomal matrix proteins are posttranslationally imported into peroxisomes with the peroxisome-targeting signal 1 receptor, Pex5. The longer isoform of Pex5, Pex5L, also transports Pex7-PTS2 protein complexes. After unloading the cargoes, Pex5 returns to the cytosol. To address molecular mechanisms underlying Pex5 functions, we constructed a cell-free Pex5 translocation system with a postnuclear supernatant fraction from CHO cell lines. In assays using the wild-type CHO-K1 cell fraction, 35S-labeled Pex5 was specifically imported into and exported from peroxisomes with multiple rounds. 35S-Pex5 import was also evident using peroxisomes isolated from rat liver. ATP was not required for 35S-Pex5 import but was indispensable for export. 35S-Pex5 was imported neither to peroxisome remnants from RING peroxin-deficient cell mutants nor to those from pex14 cells lacking a Pex5-docking site. In contrast, 35S-Pex5 was imported into the peroxisome remnants of PEX1-, PEX6-, and PEX26-defective cell mutants, including those from patients with peroxisome biogenesis disorders, from which, however, 35S-Pex5 was not exported, thereby indicating that Pex1 and Pex6 of the AAA ATPase family and their recruiter, Pex26, were essential for Pex5 export. Moreover, we analyzed the 35S-Pex5-associated complexes on peroxisomal membranes by blue-native polyacrylamide gel electrophoresis. 35S-Pex5 was in two distinct, 500- and 800-kDa complexes comprising different sets of peroxins, such as Pex14 and Pex2, implying that Pex5 transited between the subcomplexes. Together, results indicated that Pex5 most likely enters peroxisomes, changes its interacting partners, and then exits using ATP energy.
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5

Gonzalez, Kim L., Sarah E. Ratzel, Kendall H. Burks, Charles H. Danan, Jeanne M. Wages, Bethany K. Zolman, and Bonnie Bartel. "A pex1 missense mutation improves peroxisome function in a subset of Arabidopsis pex6 mutants without restoring PEX5 recycling." Proceedings of the National Academy of Sciences 115, no. 14 (March 19, 2018): E3163—E3172. http://dx.doi.org/10.1073/pnas.1721279115.

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Peroxisomes are eukaryotic organelles critical for plant and human development because they house essential metabolic functions, such as fatty acid β-oxidation. The interacting ATPases PEX1 and PEX6 contribute to peroxisome function by recycling PEX5, a cytosolic receptor needed to import proteins targeted to the peroxisomal matrix. Arabidopsis pex6 mutants exhibit low PEX5 levels and defects in peroxisomal matrix protein import, oil body utilization, peroxisomal metabolism, and seedling growth. These defects are hypothesized to stem from impaired PEX5 retrotranslocation leading to PEX5 polyubiquitination and consequent degradation of PEX5 via the proteasome or of the entire organelle via autophagy. We recovered a pex1 missense mutation in a screen for second-site suppressors that restore growth to the pex6-1 mutant. Surprisingly, this pex1-1 mutation ameliorated the metabolic and physiological defects of pex6-1 without restoring PEX5 levels. Similarly, preventing autophagy by introducing an atg7-null allele partially rescued pex6-1 physiological defects without restoring PEX5 levels. atg7 synergistically improved matrix protein import in pex1-1 pex6-1, implying that pex1-1 improves peroxisome function in pex6-1 without impeding autophagy of peroxisomes (i.e., pexophagy). pex1-1 differentially improved peroxisome function in various pex6 alleles but worsened the physiological and molecular defects of a pex26 mutant, which is defective in the tether anchoring the PEX1–PEX6 hexamer to the peroxisome. Our results support the hypothesis that, beyond PEX5 recycling, PEX1 and PEX6 have additional functions in peroxisome homeostasis and perhaps in oil body utilization.
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Titorenko, V. I., D. M. Ogrydziak, and R. A. Rachubinski. "Four distinct secretory pathways serve protein secretion, cell surface growth, and peroxisome biogenesis in the yeast Yarrowia lipolytica." Molecular and Cellular Biology 17, no. 9 (September 1997): 5210–26. http://dx.doi.org/10.1128/mcb.17.9.5210.

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We have identified and characterized mutants of the yeast Yarrowia lipolytica that are deficient in protein secretion, in the ability to undergo dimorphic transition from the yeast to the mycelial form, and in peroxisome biogenesis. Mutations in the SEC238, SRP54, PEX1, PEX2, PEX6, and PEX9 genes affect protein secretion, prevent the exit of the precursor form of alkaline extracellular protease from the endoplasmic reticulum, and compromise peroxisome biogenesis. The mutants sec238A, srp54KO, pex2KO, pex6KO, and pex9KO are also deficient in the dimorphic transition from the yeast to the mycelial form and are affected in the export of only plasma membrane and cell wall-associated proteins specific for the mycelial form. Mutations in the SEC238, SRP54, PEX1, and PEX6 genes prevent or significantly delay the exit of two peroxisomal membrane proteins, Pex2p and Pex16p, from the endoplasmic reticulum en route to the peroxisomal membrane. Mutations in the PEX5, PEX16, and PEX17 genes, which have previously been shown to be essential for peroxisome biogenesis, affect the export of plasma membrane and cell wall-associated proteins specific for the mycelial form but do not impair exit from the endoplasmic reticulum of either Pex2p and Pex16p or of proteins destined for secretion. Biochemical analyses of these mutants provide evidence for the existence of four distinct secretory pathways that serve to deliver proteins for secretion, plasma membrane and cell wall synthesis during yeast and mycelial modes of growth, and peroxisome biogenesis. At least two of these secretory pathways, which are involved in the export of proteins to the external medium and in the delivery of proteins for assembly of the peroxisomal membrane, diverge at the level of the endoplasmic reticulum.
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Chang, C. C., S. South, D. Warren, J. Jones, A. B. Moser, H. W. Moser, and S. J. Gould. "Metabolic control of peroxisome abundance." Journal of Cell Science 112, no. 10 (May 15, 1999): 1579–90. http://dx.doi.org/10.1242/jcs.112.10.1579.

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Zellweger syndrome and related disorders represent a group of lethal, genetically heterogeneous diseases. These peroxisome biogenesis disorders (PBDs) are characterized by defective peroxisomal matrix protein import and comprise at least 10 complementation groups. The genes defective in seven of these groups and more than 90% of PBD patients are now known. Here we examine the distribution of peroxisomal membrane proteins in fibroblasts from PBD patients representing the seven complementation groups for which the mutant gene is known. Peroxisomes were detected in all PBD cells, indicating that the ability to form a minimal peroxisomal structure is not blocked in these mutants. We also observed that peroxisome abundance was reduced fivefold in PBD cells that are defective in the PEX1, PEX5, PEX12, PEX6, PEX10, and PEX2 genes. These cell lines all display a defect in the import of proteins with the type-1 peroxisomal targeting signal (PTS1). In contrast, peroxisome abundance was unaffected in cells that are mutated in PEX7 and are defective only in the import of proteins with the type-2 peroxisomal targeting signal. Interestingly, a fivefold reduction in peroxisome abundance was also observed for cells lacking either of two PTS1-targeted peroxisomal beta-oxidation enzymes, acyl-CoA oxidase and 2-enoyl-CoA hydratase/D-3-hydroxyacyl-CoA dehydrogenase. These results indicate that reduced peroxisome abundance in PBD cells may be caused by their inability to import these PTS1-containing enzymes. Furthermore, the fact that peroxisome abundance is influenced by peroxisomal 105-oxidation activities suggests that there may be metabolic control of peroxisome abundance.
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8

Knoops, Kèvin, Selvambigai Manivannan, Małgorzata N. Cepińska, Arjen M. Krikken, Anita M. Kram, Marten Veenhuis, and Ida J. van der Klei. "Preperoxisomal vesicles can form in the absence of Pex3." Journal of Cell Biology 204, no. 5 (March 3, 2014): 659–68. http://dx.doi.org/10.1083/jcb.201310148.

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We demonstrate that the peroxin Pex3 is not required for the formation of peroxisomal membrane structures in yeast pex3 mutant cells. Notably, pex3 mutant cells already contain reticular and vesicular structures that harbor key proteins of the peroxisomal receptor docking complex—Pex13 and Pex14—as well as the matrix proteins Pex8 and alcohol oxidase. Other peroxisomal membrane proteins in these cells are unstable and transiently localized to the cytosol (Pex10, Pmp47) or endoplasmic reticulum (Pex11). These reticular and vesicular structures are more abundant in cells of a pex3 atg1 double deletion strain, as the absence of Pex3 may render them susceptible to autophagic degradation, which is blocked in this double mutant. Contrary to earlier suggestions, peroxisomes are not formed de novo from the endoplasmic reticulum when the PEX3 gene is reintroduced in pex3 cells. Instead, we find that reintroduced Pex3 sorts to the preperoxisomal structures in pex3 cells, after which these structures mature into normal peroxisomes.
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9

Platta, Harald W., Fouzi El Magraoui, Bastian E. Bäumer, Daniel Schlee, Wolfgang Girzalsky, and Ralf Erdmann. "Pex2 and Pex12 Function as Protein-Ubiquitin Ligases in Peroxisomal Protein Import." Molecular and Cellular Biology 29, no. 20 (August 17, 2009): 5505–16. http://dx.doi.org/10.1128/mcb.00388-09.

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ABSTRACT The PTS1-dependent peroxisomal matrix protein import is facilitated by the receptor protein Pex5 and can be divided into cargo recognition in the cytosol, membrane docking of the cargo-receptor complex, cargo release, and recycling of the receptor. The final step is controlled by the ubiquitination status of Pex5. While polyubiquitinated Pex5 is degraded by the proteasome, monoubiquitinated Pex5 is destined for a new round of the receptor cycle. Recently, the ubiquitin-conjugating enzymes involved in Pex5 ubiquitination were identified as Ubc4 and Pex4 (Ubc10), whereas the identity of the corresponding protein-ubiquitin ligases remained unknown. Here we report on the identification of the protein-ubiquitin ligases that are responsible for the ubiquitination of the peroxisomal protein import receptor Pex5. It is demonstrated that each of the three RING peroxins Pex2, Pex10, and Pex12 exhibits ubiquitin-protein isopeptide ligase activity. Our results show that Pex2 mediates the Ubc4-dependent polyubiquitination whereas Pex12 facilitates the Pex4-dependent monoubiquitination of Pex5.
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Judy, Ryan M., Connor J. Sheedy, and Brooke M. Gardner. "Insights into the Structure and Function of the Pex1/Pex6 AAA-ATPase in Peroxisome Homeostasis." Cells 11, no. 13 (June 29, 2022): 2067. http://dx.doi.org/10.3390/cells11132067.

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The AAA-ATPases Pex1 and Pex6 are required for the formation and maintenance of peroxisomes, membrane-bound organelles that harbor enzymes for specialized metabolism. Together, Pex1 and Pex6 form a heterohexameric AAA-ATPase capable of unfolding substrate proteins via processive threading through a central pore. Here, we review the proposed roles for Pex1/Pex6 in peroxisome biogenesis and degradation, discussing how the unfolding of potential substrates contributes to peroxisome homeostasis. We also consider how advances in cryo-EM, computational structure prediction, and mechanisms of related ATPases are improving our understanding of how Pex1/Pex6 converts ATP hydrolysis into mechanical force. Since mutations in PEX1 and PEX6 cause the majority of known cases of peroxisome biogenesis disorders such as Zellweger syndrome, insights into Pex1/Pex6 structure and function are important for understanding peroxisomes in human health and disease.
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Dissertations / Theses on the topic "PEX1"

1

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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2

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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3

Ciniawsky, Susanne. "Structural and functional insights into the mechanism of the Pex1/6 complex." Diss., Ludwig-Maximilians-Universität München, 2015. http://nbn-resolving.de/urn:nbn:de:bvb:19-183979.

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Peroxisomes are highly dynamic organelles of eukaryotic cells, carrying out essential oxidative metabolic processes. These organelles scavenge reactive oxygen species such as hydrogen peroxide (H2O2) and catabolise fatty acids, which are particular hallmarks and highly conserved features of peroxisomes among different species. Peroxisomal proteins and enzymes are encoded by nuclear DNA and therefore, targeted post-translationally into the peroxisomal matrix. A special class of proteins, collectively called peroxins, perform certain cellular tasks, such as peroxisomal matrix protein import or membrane development in order to maintain peroxisome biogenesis as well as a constant flux of matrix proteins into peroxisomes. The type II AAA+ peroxins Pex1/Pex6 are a core component of the peroxisomal matrix protein import system. ATPases of the AAA+ family of proteins generally assemble into large, macromolecular machines, structurally remodelling their substrate protein, which is driven by the hydrolysis of ATP. The main function of Pex1/6 complexes is to release the receptor Pex5 from peroxisomal membranes after matrix protein import. This relocation of Pex5 into the cytosol ensures a constant pool of available receptor molecules for subsequent cycles of protein import into peroxisomes. Accordingly, certain mutations in mammalian Pex1/Pex6 proteins compromise peroxisome biogenesis and thus, lipid metabolism, causing severe genetic Zellweger diseases in humans. In collaboration with Professor Ralf Erdmann and colleagues at the Ruhr-Universität Bochum, we characterize the structure and function of the AAA+ Pex1/6 complex from yeast Saccharomyces cerevisiae. Single particle electron microscopy (EM) in combination with biochemical assays allows us to analyze how ATP turnover is related to the biological function of the Pex1/6 complex. This study presents EM structures of Pex1/6 complexes assembled in the presence of ADP, ATP, ADP-AlFx and ATPγS, providing a comprehensive structural characterization of the heterohexameric type II AAA+ complex in different nucleotide states. Our EM reconstructions reveal an unexpected triangular overall shape, different than observed for the closely related and well-characterized homohexameric AAA+ protein p97. We show that the heterohexameric Pex1/6 complex is composed of a trimer of heterodimers with alternating subunit arrangement of Pex1 and Pex6 moieties. Furthermore, our results suggest that conserved aromatic residues, lining the central pore of the Pex1/6 D2 ring mediate substrate interactions. These residues correspond to substrate interaction regions in related AAA+ proteins. Comparing Pex1/6 EM reconstructions in different nucleotide states implicates that the mechanical function of Pex1/6 involves an N- to C-terminal protein translocation mechanism along the central pore. The Pex1/6 EM structures resolve symmetric and asymmetric large-scale domain motions, which likely create a power stroke during cycles of ATP binding and hydrolysis. We conclude that Pex5 is probably partially or completely unfolded while it is threaded through the central pore of Pex1/6 complexes. In addition, ATP hydrolysis assays of Pex1/Pex6 complexes containing single amino acid exchanges in individual Walker B motifs reveal that not all active sites are functionally equivalent. In isolated complexes, ATP turnover mainly occurs in Pex6 D2 domains, while Pex1 subunits sustain the structural integrity of the complex. We further resolve the structures of Pex1/6 Walker B variants and observe mutually exclusive protomer-protomer communication. In the Pex1/6 complex, a Walker B mutation induces ATP hydrolysis in the adjacent D2 domain, presenting a structural framework of protomer-protomer communication in the AAA+ heterohexamer.
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Prestele, Jakob. "Funktionelle Charakterisierung der pflanzlichen Zink-RING-Finger-Peroxine PEX10, PEX2 und PEX12 in Arabidopsis thaliana." kostenfrei, 2009. http://d-nb.info/998641693/34.

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MacLean, Gillian. "Recovery of PEX1-Gly843Asp associated peroxisome dysfunction by flavonoid compounds in fibroblasts from Zellweger spectrum patients." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114521.

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Zellweger spectrum disorder (ZSD) is due to defects in any one of 13 PEX proteins, encoded by PEX genes, which are required for peroxisome biogenesis. ZSD features neurologic, hepatic and renal abnormalities; however, one common mutation, PEX1-p.Gly843Asp (G843D), confers a milder phenotype and represents 30% of all ZSD alleles. Thus, identifying treatments for this allele will benefit many patients. We recently showed that PEX1-G843D behaves as a misfolded protein amendable to improved function by chemical and pharmacologic chaperones. In a small molecule screen, we reported recovery of peroxisomal matrix enzyme import by acacetin diacetate, a flavonoid that may bind to the ATP binding site of PEX1-G843D to improve conformation. In order to develop a lead compound from this library 'hit', we evaluated an additional 34 flavonoids for peroxisomal matrix enzyme import recovery using a patient fibroblast cell line hemizygous for PEX1-G843D and expressing a GFP-tagged peroxisome targeting signal (PTS1-GFP reporter). Eight flavonoids were identified as potential pharmacologic chaperones. Based on these compounds, additional flavonoid derivatives were produced and tested to determine the minimal pharmacophore. Relevant functional groups that enhanced or decreased efficacy were identified from these compounds, with diosmetin as the most effective one. These findings will aid in determining structure activity relationships, as knowledge of chemicals that are effective and ineffective will be used to determine the interactions that are important in developing a pharmacophore model. To determine how the flavonoids may be affecting PEX1 and associated proteins, PEX6 and PEX5, subcellular fractions were analyzed by SDS-PAGE and Blue Native PAGE to evaluate protein localization and complex formation. This was first done in wild type and various null cell lines to determine what to expect in normal and diseased states. It was found that PEX1 and PEX6 are dependent on each other and on PEX26 for stable levels and peroxisomal localization, and that PEX5 is dependent on these three proteins for stable levels and cytosolic localization. It was also determined that PEX1 is present in the cytosolic fraction as a monomer and a trimer, and in the peroxisomal fraction as a hexamer and dodecamer. Flavonoid treatment did not appear to affect the localization of PEX1 or PEX6 or complex formation. Thus, we propose that the flavonoids interact with a partially folded population of PEX1 that is already able to interact with PEX6 and localize to the peroxisomal membrane. In addition, we propose that this interaction of protein and drug enhances the residual ATPase activity of the PEX1 complex, thus improving matrix protein import, as observed in the cell-based experiments.
Le trouble du spectre de Zellweger (Zellweger Spectrum Disorder – ZSD) est dû à des defaults dans l'une des treize protéines PEX, codées par les gènes PEX, nécessaires pour la biogenèse des péroxysomes. ZSD a des caractéristiques neurologiques, hépatiques et des anomalies rénales. Cependant, une mutation fréquente, PEX1-p.Gly843Asp (G843D), confère un phénotype moins sévère et représente 30% de l'ensemble des allèles ZSD. Ainsi, l'identification de traitements pour cet allèle sera bénéfique à de nombreux patients. Nous avons récemment montré que PEX1-G843D se comporte comme une protéine mal conformée, dont la fonction peut-être améliorée par des protéines chaperons chimiques ou pharmacologiques. En examinant une série de petites molécules, nous avons observé une amélioration dans l'importation d'enzyme de la matrice du péroxysome par le diacétate d'acacétine, un flavonoïde qui peut interagir avec le site de liaison de l'ATP de PEX1-G843D, afin d'améliorer sa conformation. Afin de développer un composé de base à partir de cette bibliothèque de molécules, nous avons évalué trente-quatre autres flavonoïdes pour l'amélioration de l'importation d'enzyme de la matrice péroxysomale en utilisant une lignée de fibroblastes d'un patient hémizygote pour PEX1-G843D et qui exprime un signal de ciblage péroxysomal GFP (rapporteur PTS1-GFP). Huit flavonoïdes ont été identifiés en tant que protéines chaperons pharmacologiques potentielles. En utilisant ces composés comme base, des dérivés supplémentaires de flavonoïdes ont été produits et testés afin de déterminer le pharmacophore minimal. Les groupes fonctionnels pertinents, qui accroissent ou diminuent l'efficacité, ont été identifiés à partir de ces composés, la diosmétine étant la plus efficace. Ces résultats permettront d'élucider les relations structure-activité, de même qu'une notion des produits importants dans le développement d'un modèle de pharmacophore.Afin de déterminer comment les flavonoïdes pourraient affecter PEX1 et les protéines associées, PEX5 et PEX6, des fractions subcellulaires ont été analysées par SDS-PAGE et PAGE Bleu Natif, pour évaluer la localisation des protéines et la formation de complexe. Ceci fut tout d'abord effectué à l'aide de lignées nulles et de type sauvage, pour avoir une idée des états normaux et pathologiques. Il a été constaté que PEX1 et PEX6 sont dépendantes l'une de l'autre ainsi que de PEX26 pour leur stabilité et une localisation péroxysomale, et que PEX5 est dépendante de ces trois protéines pour sa stabilité et une localisation cytosolique. Il a été déterminé que PEX1 est présente dans la fraction cytosolique à l'état de monomère et de trimère, et dans la fraction péroxysomale à l'état d'hexamère et de dodécamère. Le traitement aux flavonoïdes n'a pas l'air d'avoir un effet sur la localisation de PEX1 et PEX6 ou sur la formation de complexe. Ainsi, nous proposons que les flavonoïdes interagissent avec une population de PEX1 qui a une mauvaise conformation, et qui est capable d'interagir avec PEX6 et de se localiser à la membrane péroxysomale. De plus, nous proposons que cette interaction protéine-composé améliore l'activité ATPase résiduelle du complexe PEX1, améliorant ainsi l'importation de protéines de la matrice, comme observé dans les expériences in vitro.
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Ciniawsky, Susanne [Verfasser], and Petra [Akademischer Betreuer] Wendler. "Structural and functional insights into the mechanism of the Pex1/6 complex / Susanne Ciniawsky. Betreuer: Petra Wendler." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2015. http://d-nb.info/1075456509/34.

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Heldt, Katrin [Verfasser], Ralf [Gutachter] Erdmann, and Ingvild [Gutachter] Birschmann. "Die Rolle der Peroxine PEX3, PEX16 und PEX19 im Rahmen der Biogenese von Peroxisomen beim Menschen / Katrin Heldt ; Gutachter: Ralf Erdmann, Ingvild Birschmann ; Medizinische Fakultät." Bochum : Ruhr-Universität Bochum, 2021. http://d-nb.info/1236813839/34.

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Soukupová, Monika. "Biogenese von Peroxisomen Untersuchungen zu PEX3- und PEX5-Proteinen des Menschen /." [S.l. : s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=959508287.

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Nguyen, Tam Hong. "Pex13 Mutant Mice as Models for the Peroxisome Biogenesis Disorders." Thesis, Griffith University, 2008. http://hdl.handle.net/10072/366797.

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Zellweger syndrome (ZS) is the most severe form of a spectrum of disorders resulting from mutations in PEX genes, genes that encode proteins necessary for peroxisome biogenesis. Loss of functional peroxiosmes leads to disruption of multiple metabolic pathways involving the peroxisome, including very long chain fatty acid oxidation and plasmalogen and bile acid synthesis. ZS patients exhibit a range of clinical abnormalities, including facial dysmorphism, cataracts, hypotonia, seizures, psychomotor retardation, and hearing impairment. In terms of tissue pathology, there are also wide ranging effects, including neuronal migration defects, hepatomegaly, retinopathy, and renal cysts. Pex13 encodes a peroxisomal membrane protein that is essential for peroxisome biogenesis. Previous work in this laboratory resulted in the generation of a Pex13-null mouse model for the purpose of investigating the pathogenesis of Zellweger syndrome. The work in the first part of this thesis extends these studies and describes the generation and initial characterisation of tissue-specific Pex13 mouse models. These tissue-specific models are expected be useful tools for analysis of the impact of localised, brain- and liver-specific elimination of peroxisomes on the pathogenesis of ZS. In addition, in the second part of the thesis, a separate and novel hypothesis is addressed as an explanation for the molecular pathogenesis of ZS, through investigating the relationship between reduced peroxisome abundance and microtubule-mediated peroxisome trafficking. Pex13 brain mutant mice were generated by mating the previously generated Pex13-floxed mice with mice expressing Cre recombinase under the control of the neuron-specific rat nestin promoter. Pex13 brain mutant mice displayed growth retardation beginning at day 5 postnatal, with gradual deterioration until death at approximately day 22 postnatal. Other clinical features included contracted postures, under-developed lower body mass, abnormal and unsteady gait, and abnormal motor coordination. In terms of brain metabolic function, these mice exhibited significant defects in plasmalogen synthesis, but, surprisingly, VLCFA levels were similar to those of littermate control mice. Significantly, peroxisome elimination in brain resulted in increased levels of plasmalogen levels in liver of Pex13 brain mutant mice. Consistent with the expected pathology resulting from deficiency of brain peroxisomes, brain mutants exhibited defective neuronal migration characterised by increased cellular density in the intermediate zone of the neocortex. Microarray analysis of total brain RNA from Pex13 brain mutants revealed several functionally-linked pathways associated with the differentially expressed genes, including cell-cell signalling, cell compromise/death, lipid metabolism, cell movement, and serotonin synthesis.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Physical Sciences
Science, Environment, Engineering and Technology
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Mayerhofer, Peter Uli. "Functional characterization of the human peroxins PEX3 and PEX19, proteins essential for early peroxisomal membrane biogenesis." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=969361378.

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Books on the topic "PEX1"

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Nduur, Baydi Tall. Dooley Pexe. [Dakar?: s.n., 1997.

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Pexe du ñàkk. Ndakaaru: OSAD, 2013.

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Baltic Sea Patchiness Experiment (1986). Baltic Sea Patchiness Experiment: PEX '86. Copenhagen, Denmark: International Council for the Exploration of the Sea, 1989.

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Rick, Turner, Hatt Deborah, Cook Jim, and International Business Machines Corporation. International Technical Support Organization., eds. Application and program performance analysis using PEX Statistics on IBM i5/OS. [Poughkeepsie, NY]: IBM Technical support Organization, 2007.

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Delille, Hannah Katharina. Biogenesis of peroxisomes in mammalian cells: Characterization of the Pex11 proteins and their role in peroxisomal growth and division. Marburg: Philipps-Universität Marburg, 2011.

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International, Creative Publishing. The complete guide to plumbing: Faucets & fixtures - PEX - tubs & toilets - water heaters? troubleshooting & repair - much more. 5th ed. Minneapolis, Minn: Creative Pub. International, 2012.

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Distrito Electoral para Los Pex. Lulu Press, Inc., 2012.

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Inc, Bergwall Productions. PE41 Troubleshooting PC Hardware-Activity Sheets (1O Package). Delmar Pub, 1998.

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NA. Amer Peop Vol 1& Voices Am Peo1& Mhl CC Pkg. Addison Wesley Publishing Company, 2006.

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Swanson, Gordon. Αpex Legends - COLORING BOOK - Collection of Selected Illustrations for Coloring. Independently Published, 2022.

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Book chapters on the topic "PEX1"

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Muntau, Ania C., Adelbert A. Roscher, Wolf-H. Kunau, and Gabriele Dodt. "Interaction of PEX3 and PEX19 Visualized by Fluorescence Resonance Energy Transfer (FRET)." In Advances in Experimental Medicine and Biology, 221–24. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9072-3_27.

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Okumoto, Kanji, Non Miyata, and Yukio Fujiki. "Identification of Peroxisomal Protein Complexes with PTS Receptors, Pex5 and Pex7, in Mammalian Cells." In Proteomics of Peroxisomes, 287–98. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-2233-4_12.

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Parmentier, Richard J. "Charles S. Peirce." In Handbook of Pragmatics, 1–18. Amsterdam: John Benjamins Publishing Company, 1999. http://dx.doi.org/10.1075/hop.3.pei1.

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Lindsay, Roger. "Perception and language." In Handbook of Pragmatics, 1–20. Amsterdam: John Benjamins Publishing Company, 2003. http://dx.doi.org/10.1075/hop.7.per1.

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Thomas, Spencer W. "X and PEX Programming." In Advances in Computer Graphics, 269–307. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76286-4_7.

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Kniestedt, Christoph. "PEX Glaukom bei Alzheimerpatientin." In Fallbeispiele Augenheilkunde, 79–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-42219-5_22.

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Richter, Michael M. "Eine prozedurale Variante: PEX." In Diagnose von technischen Systemen, 91–114. Wiesbaden: Deutscher Universitätsverlag, 1993. http://dx.doi.org/10.1007/978-3-663-14645-2_6.

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de Halleux, Jonathan, and Nikolai Tillmann. "Parameterized Unit Testing with Pex." In Tests and Proofs, 171–81. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-79124-9_12.

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De Maio, Giancarlo, Alexandros Kapravelos, Yan Shoshitaishvili, Christopher Kruegel, and Giovanni Vigna. "PExy: The Other Side of Exploit Kits." In Detection of Intrusions and Malware, and Vulnerability Assessment, 132–51. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08509-8_8.

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Tillmann, Nikolai, Jonathan de Halleux, and Wolfram Schulte. "Parameterized Unit Testing with Pex: Tutorial." In Lecture Notes in Computer Science, 141–202. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-14335-9_5.

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Conference papers on the topic "PEX1"

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"Targeting peroxisomal transport in trypanosoma." In 4th International Conference on Biological & Health Sciences (CIC-BIOHS’2022). Cihan University, 2022. http://dx.doi.org/10.24086/biohs2022/paper.566.

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Human infection with Trypanosoma parasites (Chagas disease and Human African Trypanosomiasis) affects around 10 million people worldwide resulting in life-threatening disease. Treatment options are limited to historic drugs characterized by significant side effects and decreasing efficacy while new drug development efforts are largely neglected. Here, we review drug discovery effort in human trypanosomiasis undertaken in academia. Peroxisomal (Pex) transport system was validated as a target in Chagas disease and a number of compounds were delivered which have shown promising results in animal experiments. Future perspectives of exploring the Pex system in anti-trypanosoma drug development are discussed.
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Kwon, Oh-Yang, Jung-Kyu Jun, and Yuris A. Dzenis. "Nondestructive Methods for the Damage Assessment of Cylindrically Curved Composite Laminates Subjected to Low-Velocity Impact." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-33430.

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Curved composite laminates appeared to be more vulnerable than flat ones to rapid transverse loading. Damage induced by low-velocity impact on the cylindrically curved composite laminates has been experimentally investigated. Graphite/epoxy shells with the radius of curvatures of 150 mm showed quite different impact response and damage behavior from that of flat laminate. Under the same impact energy level, the maximum contact force varied with the radius of curvatures, which is directly related to the impact damage. Delamination was distributed rather evenly at each interface along the thickness direction of curved laminates on the contrary to the case of flat laminates, where delamination is typically concentrated at the interfaces away from the impact point. Due to the presence of curvature, the acoustic microscopy could not be directly applied to the layer-by-layer assessment of delamination damage. As an alternative, the penetrant-enhanced X-radiography (PEXR) was introduced and the results from PEXR were compared with those from destructive examination of the cross-section by scanning electron microscopy.
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HyunYong Lee and Akihiro Nakao. "Topology-aware PEX for improving BitTorrent." In 38th Annual IEEE Conference on Local Computer Networks (LCN 2013). IEEE, 2013. http://dx.doi.org/10.1109/lcn.2013.6761306.

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Juusela, Maria, Venla Aaltonen, Seppo Sarna, Erik Qvist, and Kristiina Malmström. "Particles in exhaled air (PExA) method - repeatability in children." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa1705.

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Traini Ferreira, Armando, César Henrique Britto Nascimento, and Takashi Uehara. "DECAIMENTO DE TEMPERATURA EM TUBULAÇÕES PEX PARA CONDUÇÃO DE ÁGUA QUENTE." In XIV SIMPÓSIO NACIONAL DE SISTEMAS PREDIAIS [SISPRED 2021]. Antac, 2021. http://dx.doi.org/10.46421/sispred.v2i.855.

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RESUMO: O Polietileno Reticulado (PEX) é um material flexível utilizado no mercado da construção civil em sistemas prediais de água quente e fria, e assim como outros materiais, ao conduzir água quente, perde temperatura entre o ponto inicial e o ponto final de um trecho analisado, ocasionando perda de energia em forma de calor para o ambiente. Este artigo tem como objetivo verificar o comportamento do decaimento de temperatura em tubulações PEX de água quente de diversos diâmetros e fornecer essas informações para as fichas técnicas e os projetistas, para isto, serão adotados métodos iterativos e de simulação. Utilizando o software de simulação como parâmetro, obteve-se que o DN16 perdeu 0,32°C, DN20 0,17°C, DN25 0,11°C e DN32 0,07°C de temperatura em um trecho de 1 m de comprimento. Assim, é possível conhecer o decaimento de temperatura em determinadas distâncias, fator que auxilia o projetista na escolha do tamanho da tubulação a ser projetada de acordo com o diâmetro, para uma vazão fixada.
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Zhang, Chunyang, Gaogang Xie, and Peng He. "PextCuts: A High-performance Packet Classification Algorithm with Pext CPU Instruction." In 2022 IEEE/ACM 30th International Symposium on Quality of Service (IWQoS). IEEE, 2022. http://dx.doi.org/10.1109/iwqos54832.2022.9812873.

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Juusela, Maria, Kristiina Malmström, Venla Aaltonen, Seppo Sarna, and Erik Qvist. "Particles in exhaled air (PExA) in assessment of asthma in children." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa5442.

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Schulte, Wolfram. "Pex--An Intelligent Assistant for Rigorous Developer Testing." In 12th IEEE International Conference on Engineering Complex Computer Systems (ICECCS 2007). IEEE, 2007. http://dx.doi.org/10.1109/iceccs.2007.35.

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Golembiewski, Cara M., Raymond G. Cruddace, and Michael P. Kowalski. "Collimator design for the J-PEX sounding rocket." In SPIE's International Symposium on Optical Science, Engineering, and Instrumentation, edited by Oswald H. W. Siegmund and Mark A. Gummin. SPIE, 1998. http://dx.doi.org/10.1117/12.330277.

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Paulovich, Fernando V., Roberto Pinho, Charl P. Botha, Anton Heijs, and Rosane Minghim. "PEx-WEB: Content-based Visualization of Web Search Results." In 2008 12th International Conference Information Visualisation (IV). IEEE, 2008. http://dx.doi.org/10.1109/iv.2008.94.

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Reports on the topic "PEX1"

1

Smith, Alice Iulia, and Fritzgerald Evans Sandoval. CMRR PEI1 XRD Project Rigaku SmartLab Review. Office of Scientific and Technical Information (OSTI), September 2017. http://dx.doi.org/10.2172/1392787.

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Gaylord, J. LYNM PE1 Surface Station List Rev1. Office of Scientific and Technical Information (OSTI), February 2022. http://dx.doi.org/10.2172/1860642.

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Wharton, S., E. Alger, M. Brown, D. Dexheimer, and R. Newsom. LYNM PE1 Meterological Experiment 2021 Technical Report. Office of Scientific and Technical Information (OSTI), August 2021. http://dx.doi.org/10.2172/1812577.

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Gaylord, J. LYNM PE1 Data Management Implementation Plan (Rev1). Office of Scientific and Technical Information (OSTI), March 2022. http://dx.doi.org/10.2172/1879277.

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Avery, M. P. Vitrinite Reflectance (Ro) of Dispersed Organics From Mobile-Texaco-Pex, Venture B-13. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1988. http://dx.doi.org/10.4095/130505.

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Gaylord, J. NSL Support for LYNM PE1 - Phases 2 and 3 Statement of Work rev1. Office of Scientific and Technical Information (OSTI), February 2022. http://dx.doi.org/10.2172/1860641.

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Gaylord, J. NSL Support for LYNM PE1 - Phases 2 and 3 Statement of Work rev3. Office of Scientific and Technical Information (OSTI), November 2022. http://dx.doi.org/10.2172/1899423.

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Fuqua, P. D., C. J. Panetta, and J. D. Barrie. Materials on the International Space Station Experiment (MISSE): Optical Analysis of Molecular Contamination on PEC1 Tray 2. Fort Belvoir, VA: Defense Technical Information Center, February 2007. http://dx.doi.org/10.21236/ada468592.

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Avery, M. P. Vitrinite reflectance (Ro) of dispersed organic matter from Chevron-PEX-Shell Acadia K-62. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2004. http://dx.doi.org/10.4095/215480.

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Avery, M. P. Vitrinite Reflectance (Ro) On the Dispersed Organics in the Mobil-Texaco-Pex Olympia A-12. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1985. http://dx.doi.org/10.4095/129957.

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