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  • 1
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    Roles of vacuolar H+-ATPase in the oxidative stress response of Candida glabrata (2016)
    Oxford University Press
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    Publication Date: 2016-07-24
    Description: Vacuolar H + -ATPase (V-ATPase) is responsible for the acidification of eukaryotic intracellular compartments and plays an important role in oxidative stress response (OSR), but its molecular bases are largely unknown. Here, we investigated how V-ATPase is involved in the OSR by using a strain lacking VPH2 , which encodes an assembly factor of V-ATPase, in the pathogenic fungus Candida glabrata . The loss of Vph2 resulted in increased H 2 O 2 sensitivity and intracellular reactive oxygen species (ROS) level independently of mitochondrial functions. The vph2 mutant also displayed growth defects under alkaline conditions accompanied by the accumulation of intracellular ROS and these phenotypes were recovered in the presence of the ROS scavenger N-acetyl- l -cysteine. Both expression and activity levels of mitochondrial manganese superoxide dismutase (Sod2) and catalase (Cta1) were decreased in the vph2 mutant. Phenotypic analyses of strains lacking and overexpressing these genes revealed that Sod2 and Cta1 play a predominant role in endogenous and exogenous OSR, respectively. Furthermore, supplementation of copper and iron restored the expression of SOD2 specifically in the vph2 mutant, suggesting that the homeostasis of intracellular cupper and iron levels maintained by V-ATPase was important for the Sod2-mediated OSR. This report demonstrates novel roles of V-ATPase in the OSR in C. glabrata .
    Print ISSN: 1567-1356
    Electronic ISSN: 1567-1364
    Topics: Biology
    Published by Oxford University Press
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  • 2
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    Identification of ter94, Drosophila VCP, as a strong modulator of motor neuron degeneration induced by knockdown of Caz, Drosophila FUS (2014)
    Oxford University Press
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    Publication Date: 2014-06-10
    Description: In humans, mutations in the fused in sarcoma ( FUS ) gene have been identified in sporadic and familial forms of amyotrophic lateral sclerosis (ALS). Cabeza ( Caz ) is the Drosophila ortholog of human FUS . Previously, we established Drosophila models of ALS harboring Caz -knockdown. These flies develop locomotive deficits and anatomical defects in motoneurons (MNs) at neuromuscular junctions; these phenotypes indicate that loss of physiological FUS functions in the nucleus can cause MN degeneration similar to that seen in FUS-related ALS. Here, we aimed to explore molecules that affect these ALS-like phenotypes of our Drosophila models with eye-specific and neuron-specific Caz -knockdown. We examined several previously reported ALS-related genes and found genetic links between Caz and ter94 , the Drosophila ortholog of human Valosin-containing protein ( VCP ). Genetic crossing the strongest loss-of-function allele of ter94 with Caz -knockdown strongly enhanced the rough-eye phenotype and the MN-degeneration phenotype caused by Caz -knockdown. Conversely, the overexpression of wild-type ter94 in the background of Caz- knockdown remarkably suppressed those phenotypes. Our data demonstrated that expression levels of Drosophila VCP ortholog dramatically modified the phenotypes caused by Caz -knockdown in either direction, exacerbation or remission. Our results indicate that therapeutic agents that up-regulate the function of human VCP could modify the pathogenic processes that lead to the degeneration of MNs in ALS.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 3
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    D3M: detection of differential distributions of methylation levels (2016)
    Oxford University Press
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    Publication Date: 2016-07-30
    Description: Motivation: DNA methylation is an important epigenetic modification related to a variety of diseases including cancers. We focus on the methylation data from Illumina’s Infinium HumanMethylation450 BeadChip. One of the key issues of methylation analysis is to detect the differential methylation sites between case and control groups. Previous approaches describe data with simple summary statistics or kernel function, and then use statistical tests to determine the difference. However, a summary statistics-based approach cannot capture complicated underlying structure, and a kernel function-based approach lacks interpretability of results. Results: We propose a novel method D 3 M, for detection of differential distribution of methylation, based on distribution-valued data. Our method can detect the differences in high-order moments, such as shapes of underlying distributions in methylation profiles, based on the Wasserstein metric. We test the significance of the difference between case and control groups and provide an interpretable summary of the results. The simulation results show that the proposed method achieves promising accuracy and shows favorable results compared with previous methods. Glioblastoma multiforme and lower grade glioma data from The Cancer Genome Atlas show that our method supports recent biological advances and suggests new insights. Availability and Implementation: R implemented code is freely available from https://github.com/ymatts/D3M/ . Contact: ymatsui@med.nagoya-u.ac.jp or shimamura@med.nagoya-u.ac.jp Supplementary information: Supplementary data are available at Bioinformatics online.
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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  • 4
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    Statistical model-based testing to evaluate the recurrence of genomic aberrations (2012)
    Oxford University Press
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    Publication Date: 2012-06-12
    Description: Motivation: In cancer genomes, chromosomal regions harboring cancer genes are often subjected to genomic aberrations like copy number alteration and loss of heterozygosity. Given this, finding recurrent genomic aberrations is considered an apt approach for screening cancer genes. Although several permutation-based tests have been proposed for this purpose, none of them are designed to find recurrent aberrations from the genomic dataset without paired normal sample controls. Their application to unpaired genomic data may lead to false discoveries, because they retrieve pseudo-aberrations that exist in normal genomes as polymorphisms. Results: We develop a new parametric method named parametric aberration recurrence test (PART) to test for the recurrence of genomic aberrations. The introduction of Poisson-binomial statistics allow us to compute small P -values more efficiently and precisely than the previously proposed permutation-based approach. Moreover, we extended PART to cover unpaired data (PART-up) so that there is a statistical basis for analyzing unpaired genomic data. PART-up uses information from unpaired normal sample controls to remove pseudo-aberrations in unpaired genomic data. Using PART-up, we successfully predict recurrent genomic aberrations in cancer cell line samples whose paired normal sample controls are unavailable. This article thus proposes a powerful statistical framework for the identification of driver aberrations, which would be applicable to ever-increasing amounts of cancer genomic data seen in the era of next generation sequencing. Availability: Our implementations of PART and PART-up are available from http://www.hgc.jp/~niiyan/PART/manual.html . Contact: aniida@ims.u-tokyo.ac.jp Supplementary information: Supplementary data are available at Bioinformatics online.
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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  • 5
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    Systems biology analysis of Drosophila in vivo screen data elucidates core networks for DNA damage repair in SCA1 (2014)
    Oxford University Press
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    Publication Date: 2014-02-08
    Description: DNA damage repair is implicated in neurodegenerative diseases; however, the relative contributions of various DNA repair systems to the pathology of these diseases have not been investigated systematically. In this study, we performed a systematic in vivo screen of all available Drosophila melanogaster homolog DNA repair genes, and we tested the effect of their overexpression on lifespan and developmental viability in Spinocerebellar Ataxia Type 1 (SCA1) Drosophila models expressing human mutant Ataxin-1 (Atxn1). We identified genes previously unknown to be involved in CAG-/polyQ-related pathogenesis that function in multiple DNA damage repair systems. Beyond the significance of each repair system, systems biology analyses unraveled the core networks connecting positive genes in the gene screen that could contribute to SCA1 pathology. In particular, RpA1, which had the largest effect on lifespan in the SCA1 fly model, was located at the hub position linked to such core repair systems, including homologous recombination (HR). We revealed that Atxn1 actually interacted with RpA1 and its essential partners BRCA1/2. Furthermore, mutant but not normal Atxn1 impaired the dynamics of RpA1 in the nucleus after DNA damage. Uptake of BrdU by Purkinje cells was observed in mutant Atxn1 knockin mice, suggesting their abnormal entry to the S-phase. In addition, chemical and genetic inhibitions of Chk1 elongated lifespan and recovered eye degeneration. Collectively, we elucidated core networks for DNA damage repair in SCA1 that might include the aberrant usage of HR.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 6
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    Statistical model-based testing to evaluate the recurrence of genomic aberrations (2012)
    Oxford University Press
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    Publication Date: 2012-06-11
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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  • 7
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    El Tor hemolysin of O1 forms channels in planar lipid bilayer membranes (1997)
    Oxford University Press
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    Publication Date: 1997-05-15
    Print ISSN: 0378-1097
    Electronic ISSN: 1574-6968
    Topics: Biology
    Published by Oxford University Press on behalf of Federation of European Microbiological Societies.
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