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Mutations in CHMP2B in Lower Motor Neuron Predominant Amyotrophic Lateral Sclerosis (ALS)
This is a repository copy of Mutations in CHMP2B in lower motor neuron predominant amyotrophic lateral sclerosis (ALS). White Rose Research Online URL for this paper: http://eprints.whiterose.ac.uk/10846/ Article: Cox, L.E., Ferraiuolo, L., Goodall, E.F. et al. (13 more authors) (2010) Mutations in CHMP2B in lower motor neuron predominant amyotrophic lateral sclerosis (ALS). Plos One, 5 (3). Art no.e9872. ISSN 1932-6203 https://doi.org/10.1371/journal.pone.0009872 Reuse Unless indicated otherwise, fulltext items are protected by copyright with all rights reserved. The copyright exception in section 29 of the Copyright, Designs and Patents Act 1988 allows the making of a single copy solely for the purpose of non-commercial research or private study within the limits of fair dealing. The publisher or other rights-holder may allow further reproduction and re-use of this version - refer to the White Rose Research Online record for this item. Where records identify the publisher as the copyright holder, users can verify any specific terms of use on the publisher’s website. Takedown If you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing [email protected] including the URL of the record and the reason for the withdrawal request. [email protected] https://eprints.whiterose.ac.uk/ Mutations in CHMP2B in Lower Motor Neuron Predominant Amyotrophic Lateral Sclerosis (ALS) Laura E. Cox1, Laura Ferraiuolo1, Emily F. Goodall1, Paul R. Heath1, Adrian Higginbottom1, Heather Mortiboys1, Hannah C. Hollinger1, Judith A. Hartley1, Alice Brockington1, Christine E. -
Genetic Screen Identifies Serpin5 As a Regulator of the Toll Pathway and CHMP2B Toxicity Associated with Frontotemporal Dementia
Genetic screen identifies serpin5 as a regulator of the toll pathway and CHMP2B toxicity associated with frontotemporal dementia S. Tariq Ahmada, Sean T. Sweeneyb, Jin-A Leea, Neal T. Sweeneya,c,1, and Fen-Biao Gaoa,c,2 aGladstone Institute of Neurological Disease, San Francisco, CA 94158; bDepartment of Biology, University of York, P.O. Box 373, York YO10 5YW, United Kingdom; and cNeuroscience Graduate Program, University of California, San Francisco, CA 94158 Edited by Yuh Nung Jan, University of California School of Medicine, San Francisco, CA, and approved May 18, 2009 (received for review March 23, 2009) Frontotemporal dementia (FTD) is the most common form of demen- gain-of-function mechanism. However, animal models of FTD3 tia before 60 years of age. Rare pathogenic mutations in CHMP2B, have not been reported, and the signaling pathways that are which encodes a component of the endosomal sorting complex misregulated in vivo remain to be identified. required for transport (ESCRT-III), are associated with FTD linked to In recent years, Drosophila models have been instrumental in chromosome 3 (FTD3). Animal models of FTD3 have not yet been uncovering molecular pathways that contribute to the pathogenesis reported, and what signaling pathways are misregulated by mutant of neurodegenerative diseases (17, 18). In this study, we modeled CHMP2B in vivo is unknown. Here we report the establishment of a the effect of CHMP2B in human FTD3 using a gain-of-function Drosophila model of FTD3 and show the genetic interactions between approach, which is similar to the approach that gives effects in mutant CHMP2B and other components of ESCRT. -
Rhoa Promotes Epidermal Stem Cell Proliferation Via PKN1-Cyclin D1 Signaling
RESEARCH ARTICLE RhoA promotes epidermal stem cell proliferation via PKN1-cyclin D1 signaling Fan Wang1, Rixing Zhan2, Liang Chen1, Xia Dai1, Wenping Wang1, Rui Guo1, Xiaoge Li1, Zhe Li1, Liang Wang1, Shupeng Huang1, Jie Shen1, Shirong Li1☯*, Chuan Cao1☯* 1 Department of Plastic and Reconstructive Surgery, Southwestern Hospital, Third Military Medical University, Chongqing, China, 2 School of Nursing, Third Military Medical University, Chongqing, China ☯ These authors contributed equally to this work. * [email protected] (LS); [email protected] (CC) a1111111111 Abstract a1111111111 a1111111111 a1111111111 a1111111111 Objective Epidermal stem cells (ESCs) play a critical role in wound healing, but the mechanism under- lying ESC proliferation is not well defined. Here, we explore the effects of RhoA on ESC pro- liferation and the possible underlying mechanism. OPEN ACCESS Citation: Wang F, Zhan R, Chen L, Dai X, Wang W, Methods Guo R, et al. (2017) RhoA promotes epidermal (+/+) (-/- stem cell proliferation via PKN1-cyclin D1 Human ESCs were enriched by rapid adhesion to collagen IV. RhoA (G14V), RhoA ) signaling. PLoS ONE 12(2): e0172613. (T19N) and pGFP control plasmids were transfected into human ESCs. The effect of RhoA doi:10.1371/journal.pone.0172613 on cell proliferation was detected by cell proliferation and DNA synthesis assays. Induction Editor: Austin John Cooney, University of Texas at of PKN1 activity by RhoA was determined by immunoblot analysis, and the effects of PKN1 Austin Dell Medical School, UNITED STATES on RhoA in terms of inducing cell proliferation and cyclin D1 expression were detected using Received: August 10, 2016 specific siRNA targeting PKN1. The effects of U-46619 (a RhoA agonist) and C3 transferase Accepted: February 6, 2017 (a RhoA antagonist) on ESC proliferation were observed in vivo. -
Angio-Associated Migratory Cell Protein Interacts with Epidermal
Cellular Signalling 61 (2019) 10–19 Contents lists available at ScienceDirect Cellular Signalling journal homepage: www.elsevier.com/locate/cellsig Angio-associated migratory cell protein interacts with epidermal growth factor receptor and enhances proliferation and drug resistance in human T non-small cell lung cancer cells Shun Yaoa, Feifei Shia, Yingying Wanga,b, Xiaoyang Suna, Wenbo Suna, Yifeng Zhanga, ⁎ ⁎ Xianfang Liuc, Xiangguo Liua,b, , Ling Sua,b, a Shandong Provincial Key Laboratory of Animal Cell and Developmental Biology, School of Life Sciences, Shandong University, Qingdao, China b Shandong Provincial Collaborative Innovation Center of Cell Biology, School of Life Sciences, Shandong Normal University, Jinan, China c The Department of Otolaryngology Head and Neck Surgery, Shandong Provincial Hospital, Affiliated to Shandong University, Jinan, China ARTICLE INFO ABSTRACT Keywords: Angio-associated migratory cell protein (AAMP) is expressed in some human cancer cells. Previous studies have AAMP shown AAMP high expression predicted poor prognosis. But its biological role in non-small cell lung cancer Proliferation (NSCLC) cells is still unknown. In our present study, we attempted to explore the functions of AAMP in NSCLC Tumorigenesis cells. According to our findings, AAMP knockdown inhibited lung cancer cell proliferation and inhibited lung EGFR cancer cell tumorigenesis in the mouse xenograft model. Epidermal growth factor receptor (EGFR) is a primary Icotinib receptor tyrosine kinase (RTK) that promotes proliferation and plays an important role in cancer pathology. We Doxorubicin found AAMP interacted with EGFR and enhanced its dimerization and phosphorylation at tyrosine 1173 which activated ERK1/2 in NSCLC cells. In addition, we showed AAMP conferred the lung cancer cells resistance to chemotherapeutic agents such as icotinib and doxorubicin. -
Role of Meprin Metalloproteases in Metastasis and Tumor Microenvironment
Cancer and Metastasis Reviews (2019) 38:347–356 https://doi.org/10.1007/s10555-019-09805-5 Role of meprin metalloproteases in metastasis and tumor microenvironment Florian Peters1 & Christoph Becker-Pauly1 Published online: 3 September 2019 # Springer Science+Business Media, LLC, part of Springer Nature 2019 Abstract A crucial step for tumor cell extravasation and metastasis is the migration through the extracellular matrix, which requires proteolytic activity. Hence, proteases, particularly matrix metalloproteases (MMPs), have been discussed as therapeutic targets and their inhibition should diminish tumor growth and metastasis. The metalloproteases meprin α and meprin β are highly abundant on intestinal enterocytes and their expression was associated with different stages of colorectal cancer. Due to their ability to cleave extracellular matrix (ECM) components, they were suggested as pro-tumorigenic enzymes. Additionally, both meprins were shown to have pro-inflammatory activity by cleaving cytokines and their receptors, which correlates with chronic intestinal inflammation and associated conditions. On the other hand, meprin β was identified as an essential enzyme for the detachment and renewal of the intestinal mucus, important to prevent bacterial overgrowth and infection. Considering this, it is hard to estimate whether high activity of meprins is generally detrimental or if these enzymes have also protective functions in certain cancer types. For instance, for colorectal cancer, patients with high meprin β expression in tumor tissue exhibit a better survival prognosis, which is completely different to prostate cancer. This demonstrates that the very same enzyme may have contrary effects on tumor initiation and growth, depending on its tissue and subcellular localization. Hence, precise knowledge about proteolytic enzymes is required to design the most efficient therapeutic options for cancer treatment. -
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Patterns of DNA methylation on the human X chromosome and use in analyzing X-chromosome inactivation by Allison Marie Cotton B.Sc., The University of Guelph, 2005 A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY in The Faculty of Graduate Studies (Medical Genetics) THE UNIVERSITY OF BRITISH COLUMBIA (Vancouver) January 2012 © Allison Marie Cotton, 2012 Abstract The process of X-chromosome inactivation achieves dosage compensation between mammalian males and females. In females one X chromosome is transcriptionally silenced through a variety of epigenetic modifications including DNA methylation. Most X-linked genes are subject to X-chromosome inactivation and only expressed from the active X chromosome. On the inactive X chromosome, the CpG island promoters of genes subject to X-chromosome inactivation are methylated in their promoter regions, while genes which escape from X- chromosome inactivation have unmethylated CpG island promoters on both the active and inactive X chromosomes. The first objective of this thesis was to determine if the DNA methylation of CpG island promoters could be used to accurately predict X chromosome inactivation status. The second objective was to use DNA methylation to predict X-chromosome inactivation status in a variety of tissues. A comparison of blood, muscle, kidney and neural tissues revealed tissue-specific X-chromosome inactivation, in which 12% of genes escaped from X-chromosome inactivation in some, but not all, tissues. X-linked DNA methylation analysis of placental tissues predicted four times higher escape from X-chromosome inactivation than in any other tissue. Despite the hypomethylation of repetitive elements on both the X chromosome and the autosomes, no changes were detected in the frequency or intensity of placental Cot-1 holes. -
Metalloproteases Meprin Α and Meprin Β Are C- and N-Procollagen Proteinases Important for Collagen Assembly and Tensile Strength
Metalloproteases meprin α and meprin β are C- and N-procollagen proteinases important for collagen assembly and tensile strength Claudia Brodera, Philipp Arnoldb, Sandrine Vadon-Le Goffc, Moritz A. Konerdingd, Kerstin Bahrd, Stefan Müllere, Christopher M. Overallf, Judith S. Bondg, Tomas Koudelkah, Andreas Tholeyh, David J. S. Hulmesc, Catherine Moalic, and Christoph Becker-Paulya,1 aUnit for Degradomics of the Protease Web, Institute of Biochemistry, University of Kiel, 24118 Kiel, Germany; bInstitute of Zoology, Johannes Gutenberg University, 55128 Mainz, Germany; cTissue Biology and Therapeutic Engineering Unit, Centre National de la Recherche Scientifique/University of Lyon, Unité Mixte de Recherche 5305, Unité Mixte de Service 3444 Biosciences Gerland-Lyon Sud, 69367 Lyon Cedex 7, France; dInstitute of Functional and Clinical Anatomy, University Medical Center, Johannes Gutenberg University, 55128 Mainz, Germany; eDepartment of Gastroenterology, University of Bern, CH-3010 Bern, Switzerland; fCentre for Blood Research, University of British Columbia, Vancouver, BC, Canada V6T 1Z3; gDepartment of Biochemistry and Molecular Biology, Pennsylvania State University College of Medicine, Hershey, PA 17033; and hInstitute of Experimental Medicine, University of Kiel, 24118 Kiel, Germany Edited by Robert Huber, Max Planck Institute of Biochemistry, Planegg-Martinsried, Germany, and approved July 9, 2013 (received for review March 22, 2013) Type I fibrillar collagen is the most abundant protein in the human formation (22). A tight balance between synthesis and break- body, crucial for the formation and strength of bones, skin, and down of ECM is required for the function of all tissues, and tendon. Proteolytic enzymes are essential for initiation of the dysregulation leads to pathophysiological events, such as arthri- assembly of collagen fibrils by cleaving off the propeptides. -
Rates and Patterns of Indels in HIV-1 Gp120 Within and Among Hosts
Western University Scholarship@Western Electronic Thesis and Dissertation Repository 8-19-2020 1:00 PM Rates and patterns of indels in HIV-1 gp120 within and among hosts John Lawrence Palmer, The University of Western Ontario Supervisor: Poon, Art F.Y., The University of Western Ontario A thesis submitted in partial fulfillment of the equirr ements for the Master of Science degree in Pathology and Laboratory Medicine © John Lawrence Palmer 2020 Follow this and additional works at: https://ir.lib.uwo.ca/etd Part of the Molecular Genetics Commons Recommended Citation Palmer, John Lawrence, "Rates and patterns of indels in HIV-1 gp120 within and among hosts" (2020). Electronic Thesis and Dissertation Repository. 7308. https://ir.lib.uwo.ca/etd/7308 This Dissertation/Thesis is brought to you for free and open access by Scholarship@Western. It has been accepted for inclusion in Electronic Thesis and Dissertation Repository by an authorized administrator of Scholarship@Western. For more information, please contact [email protected]. Abstract Insertions and deletions (indels) in the HIV-1 gp120 variable loops modulate sensitivity to neutralizing antibodies and are therefore implicated in HIV-1 immune escape. However, the rates and characteristics of variable loop indels have not been investigated within hosts. Here, I report a within-host phylogenetic analysis of gp120 variable loop indels, with mentions to my preceding study on these indels among hosts. We processed longitudinally-sampled gp120 sequences collected from a public database (n = 11,265) and the Novitsky Lab (n=2,541). I generated time-scaled within-host phylogenies using BEAST, extracted indels by reconstructing ancestral sequences in Historian, and esti- mated variable loop indel rates by applying a Poisson-based model to indel counts and time data. -
Anti-Inflammatory Role of Curcumin in LPS Treated A549 Cells at Global Proteome Level and on Mycobacterial Infection
Anti-inflammatory Role of Curcumin in LPS Treated A549 cells at Global Proteome level and on Mycobacterial infection. Suchita Singh1,+, Rakesh Arya2,3,+, Rhishikesh R Bargaje1, Mrinal Kumar Das2,4, Subia Akram2, Hossain Md. Faruquee2,5, Rajendra Kumar Behera3, Ranjan Kumar Nanda2,*, Anurag Agrawal1 1Center of Excellence for Translational Research in Asthma and Lung Disease, CSIR- Institute of Genomics and Integrative Biology, New Delhi, 110025, India. 2Translational Health Group, International Centre for Genetic Engineering and Biotechnology, New Delhi, 110067, India. 3School of Life Sciences, Sambalpur University, Jyoti Vihar, Sambalpur, Orissa, 768019, India. 4Department of Respiratory Sciences, #211, Maurice Shock Building, University of Leicester, LE1 9HN 5Department of Biotechnology and Genetic Engineering, Islamic University, Kushtia- 7003, Bangladesh. +Contributed equally for this work. S-1 70 G1 S 60 G2/M 50 40 30 % of cells 20 10 0 CURI LPSI LPSCUR Figure S1: Effect of curcumin and/or LPS treatment on A549 cell viability A549 cells were treated with curcumin (10 µM) and/or LPS or 1 µg/ml for the indicated times and after fixation were stained with propidium iodide and Annexin V-FITC. The DNA contents were determined by flow cytometry to calculate percentage of cells present in each phase of the cell cycle (G1, S and G2/M) using Flowing analysis software. S-2 Figure S2: Total proteins identified in all the three experiments and their distribution betwee curcumin and/or LPS treated conditions. The proteins showing differential expressions (log2 fold change≥2) in these experiments were presented in the venn diagram and certain number of proteins are common in all three experiments. -
Independent Apoptotic Pathways
An Sp1 transcription factor coordinates caspase- dependent and -independent apoptotic pathways The MIT Faculty has made this article openly available. Please share how this access benefits you. Your story matters. Citation Hirose, Takashi, and H. Robert Horvitz. “An Sp1 Transcription Factor Coordinates Caspase-Dependent and -Independent Apoptotic Pathways.” Nature 500, no. 7462 (July 14, 2013): 354–358. As Published http://dx.doi.org/10.1038/nature12329 Publisher Nature Publishing Group Version Author's final manuscript Citable link http://hdl.handle.net/1721.1/85566 Terms of Use Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use. Published as: Nature. 2013 August 15; 500(7462): 354–358. HHMI Author Manuscript HHMI Author Manuscript HHMI Author Manuscript An Sp1 transcription factor coordinates caspase-dependent and -independent apoptotic pathways Takashi Hirose and H. Robert Horvitz Howard Hughes Medical Institute, Department of Biology, 68-425, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA Abstract During animal development, the proper regulation of apoptosis requires the precise spatial and temporal execution of cell-death programs, which can include both caspase-dependent and caspase-independent pathways1, 2. While the mechanisms of caspase-dependent and caspase- independent cell killing have been examined extensively, how these pathways are coordinated within a single cell that is fated to die is unknown. Here we show that the C. elegans Sp1 transcription factor SPTF-3 specifies the programmed cell deaths of at least two cells, the sisters of the pharyngeal M4 motor neuron and of the AQR sensory neuron, by transcriptionally activating both caspase-dependent and caspase-independent apoptotic pathways. -
Noelia Díaz Blanco
Effects of environmental factors on the gonadal transcriptome of European sea bass (Dicentrarchus labrax), juvenile growth and sex ratios Noelia Díaz Blanco Ph.D. thesis 2014 Submitted in partial fulfillment of the requirements for the Ph.D. degree from the Universitat Pompeu Fabra (UPF). This work has been carried out at the Group of Biology of Reproduction (GBR), at the Department of Renewable Marine Resources of the Institute of Marine Sciences (ICM-CSIC). Thesis supervisor: Dr. Francesc Piferrer Professor d’Investigació Institut de Ciències del Mar (ICM-CSIC) i ii A mis padres A Xavi iii iv Acknowledgements This thesis has been made possible by the support of many people who in one way or another, many times unknowingly, gave me the strength to overcome this "long and winding road". First of all, I would like to thank my supervisor, Dr. Francesc Piferrer, for his patience, guidance and wise advice throughout all this Ph.D. experience. But above all, for the trust he placed on me almost seven years ago when he offered me the opportunity to be part of his team. Thanks also for teaching me how to question always everything, for sharing with me your enthusiasm for science and for giving me the opportunity of learning from you by participating in many projects, collaborations and scientific meetings. I am also thankful to my colleagues (former and present Group of Biology of Reproduction members) for your support and encouragement throughout this journey. To the “exGBRs”, thanks for helping me with my first steps into this world. Working as an undergrad with you Dr. -
Genome-Wide DNA Methylation Map of Human Neutrophils Reveals Widespread Inter-Individual Epigenetic Variation
www.nature.com/scientificreports OPEN Genome-wide DNA methylation map of human neutrophils reveals widespread inter-individual Received: 15 June 2015 Accepted: 29 October 2015 epigenetic variation Published: 27 November 2015 Aniruddha Chatterjee1,2, Peter A. Stockwell3, Euan J. Rodger1, Elizabeth J. Duncan2,4, Matthew F. Parry5, Robert J. Weeks1 & Ian M. Morison1,2 The extent of variation in DNA methylation patterns in healthy individuals is not yet well documented. Identification of inter-individual epigenetic variation is important for understanding phenotypic variation and disease susceptibility. Using neutrophils from a cohort of healthy individuals, we generated base-resolution DNA methylation maps to document inter-individual epigenetic variation. We identified 12851 autosomal inter-individual variably methylated fragments (iVMFs). Gene promoters were the least variable, whereas gene body and upstream regions showed higher variation in DNA methylation. The iVMFs were relatively enriched in repetitive elements compared to non-iVMFs, and were associated with genome regulation and chromatin function elements. Further, variably methylated genes were disproportionately associated with regulation of transcription, responsive function and signal transduction pathways. Transcriptome analysis indicates that iVMF methylation at differentially expressed exons has a positive correlation and local effect on the inclusion of that exon in the mRNA transcript. Methylation of DNA is a mechanism for regulating gene function in all vertebrates. It has a role in gene silencing, tissue differentiation, genomic imprinting, chromosome X inactivation, phenotypic plasticity, and disease susceptibility1,2. Aberrant DNA methylation has been implicated in the pathogenesis of sev- eral human diseases, especially cancer3–5. Variation in DNA methylation patterns in healthy individuals has been hypothesised to alter human phenotypes including susceptibility to common diseases6 and response to drug treatments7.