Comparative Expressed-Sequence-Tag Analysis of Differential Gene Expression Profiles in PC-12 Cells Before and After Nerve Growth Factor Treatment NORMAN H
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1 Evidence for Gliadin Antibodies As Causative Agents in Schizophrenia
1 Evidence for gliadin antibodies as causative agents in schizophrenia. C.J.Carter PolygenicPathways, 20 Upper Maze Hill, Saint-Leonard’s on Sea, East Sussex, TN37 0LG [email protected] Tel: 0044 (0)1424 422201 I have no fax Abstract Antibodies to gliadin, a component of gluten, have frequently been reported in schizophrenia patients, and in some cases remission has been noted following the instigation of a gluten free diet. Gliadin is a highly immunogenic protein, and B cell epitopes along its entire immunogenic length are homologous to the products of numerous proteins relevant to schizophrenia (p = 0.012 to 3e-25). These include members of the DISC1 interactome, of glutamate, dopamine and neuregulin signalling networks, and of pathways involved in plasticity, dendritic growth or myelination. Antibodies to gliadin are likely to cross react with these key proteins, as has already been observed with synapsin 1 and calreticulin. Gliadin may thus be a causative agent in schizophrenia, under certain genetic and immunological conditions, producing its effects via antibody mediated knockdown of multiple proteins relevant to the disease process. Because of such homology, an autoimmune response may be sustained by the human antigens that resemble gliadin itself, a scenario supported by many reports of immune activation both in the brain and in lymphocytes in schizophrenia. Gluten free diets and removal of such antibodies may be of therapeutic benefit in certain cases of schizophrenia. 2 Introduction A number of studies from China, Norway, and the USA have reported the presence of gliadin antibodies in schizophrenia 1-5. Gliadin is a component of gluten, intolerance to which is implicated in coeliac disease 6. -
Table 1. Identified Proteins with Expression Significantly Altered in the Hippocampus of Rats of Exposed Group (Pb) Vs
Table 1. Identified proteins with expression significantly altered in the hippocampus of rats of exposed group (Pb) vs. Control. Fold Change Accession Id a Protein Description Score Pb P35213 14-3-3 protein beta/alpha 85420 −0.835 P62260 14-3-3 protein epsilon 96570 −0.878 P68511 14-3-3 protein eta 85420 −0.844 P68255 14-3-3 protein theta 85420 −0.835 P63102 14-3-3 protein zeta/delta 105051 −0.803 P13233 2',3'-cyclic-nucleotide 3'-phosphodiesterase 151400 1.405 P68035 Actin, alpha cardiac muscle 1 442584 −0.942 P68136 Actin, alpha skeletal muscle 441060 −0.970 P62738 Actin, aortic smooth muscle 438270 −0.970 P60711 Actin, cytoplasmic 1 630104 −0.942 P63259 Actin, cytoplasmic 2 630104 −0.942 P63269 Actin, gamma-enteric smooth muscle 438270 −0.951 Q05962 ADP/ATP translocase 1 60100 −0.554 Q09073 ADP/ATP translocase 2 49102 −0.482 P84079 ADP-ribosylation factor 1 34675 −0.644 P84082 ADP-ribosylation factor 2 22412 −0.644 P61206 ADP-ribosylation factor 3 34675 −0.619 P61751 ADP-ribosylation factor 4 22412 −0.670 P84083 ADP-ribosylation factor 5 22412 −0.625 P04764 Alpha-enolase 46219 −0.951 P23565 Alpha-internexin 9478 1.062 P37377 Alpha-synuclein 89619 −0.771 P13221 Aspartate aminotransferase, cytoplasmic 23661 1.083 P00507 Aspartate aminotransferase, mitochondrial 46049 1.116 P10719 ATP synthase subunit beta, mitochondrial 232442 −0.835 P85969 Beta-soluble NSF attachment protein 9638 1.419 Q63754 Beta-synuclein 66842 −0.779 P11275 Calcium/calmodulin-dependent protein kinase type II subunit alpha 181954 1.105 P08413 Calcium/calmodulin-dependent protein kinase type II subunit beta 80840 1.127 P15791 Calcium/calmodulin-dependent protein kinase type II subunit delta 62682 1.105 Int. -
1 Metabolic Dysfunction Is Restricted to the Sciatic Nerve in Experimental
Page 1 of 255 Diabetes Metabolic dysfunction is restricted to the sciatic nerve in experimental diabetic neuropathy Oliver J. Freeman1,2, Richard D. Unwin2,3, Andrew W. Dowsey2,3, Paul Begley2,3, Sumia Ali1, Katherine A. Hollywood2,3, Nitin Rustogi2,3, Rasmus S. Petersen1, Warwick B. Dunn2,3†, Garth J.S. Cooper2,3,4,5* & Natalie J. Gardiner1* 1 Faculty of Life Sciences, University of Manchester, UK 2 Centre for Advanced Discovery and Experimental Therapeutics (CADET), Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Sciences Centre, Manchester, UK 3 Centre for Endocrinology and Diabetes, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK 4 School of Biological Sciences, University of Auckland, New Zealand 5 Department of Pharmacology, Medical Sciences Division, University of Oxford, UK † Present address: School of Biosciences, University of Birmingham, UK *Joint corresponding authors: Natalie J. Gardiner and Garth J.S. Cooper Email: [email protected]; [email protected] Address: University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, United Kingdom Telephone: +44 161 275 5768; +44 161 701 0240 Word count: 4,490 Number of tables: 1, Number of figures: 6 Running title: Metabolic dysfunction in diabetic neuropathy 1 Diabetes Publish Ahead of Print, published online October 15, 2015 Diabetes Page 2 of 255 Abstract High glucose levels in the peripheral nervous system (PNS) have been implicated in the pathogenesis of diabetic neuropathy (DN). However our understanding of the molecular mechanisms which cause the marked distal pathology is incomplete. Here we performed a comprehensive, system-wide analysis of the PNS of a rodent model of DN. -
Mechanisms of Α-Synuclein Induced Synaptopathy in Parkinson’S Disease
King’s Research Portal DOI: 10.3389/fnins.2018.00080 Document Version Publisher's PDF, also known as Version of record Link to publication record in King's Research Portal Citation for published version (APA): Bridi, J. C., & Hirth, F. (2018). Mechanisms of -Synuclein Induced Synaptopathy in Parkinson's Disease. Frontiers in Neuroscience, 12, 80. DOI: 10.3389/fnins.2018.00080 Citing this paper Please note that where the full-text provided on King's Research Portal is the Author Accepted Manuscript or Post-Print version this may differ from the final Published version. If citing, it is advised that you check and use the publisher's definitive version for pagination, volume/issue, and date of publication details. And where the final published version is provided on the Research Portal, if citing you are again advised to check the publisher's website for any subsequent corrections. General rights Copyright and moral rights for the publications made accessible in the Research Portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognize and abide by the legal requirements associated with these rights. •Users may download and print one copy of any publication from the Research Portal for the purpose of private study or research. •You may not further distribute the material or use it for any profit-making activity or commercial gain •You may freely distribute the URL identifying the publication in the Research Portal Take down policy If you believe that this document breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. -
Genbank Dennis A
D48–D53 Nucleic Acids Research, 2012, Vol. 40, Database issue Published online 5 December 2011 doi:10.1093/nar/gkr1202 GenBank Dennis A. Benson, Ilene Karsch-Mizrachi, Karen Clark, David J. Lipman, James Ostell and Eric W. Sayers* National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Building 38A, 8600 Rockville Pike, Bethesda, MD 20894, USA Received September 30, 2011; Revised November 14, 2011; Accepted November 17, 2011 ABSTRACT sequence (GSS), whole-genome shotgun (WGS) and Õ other high-throughput data from sequencing centers. GenBank is a comprehensive database that The US Office of Patents and Trademarks also contributes contains publicly available nucleotide sequences sequences from issued patents. GenBank participates with for more than 250 000 formally described species. the EMBL Nucleotide Sequence Database (EMBL-Bank), Downloaded from These sequences are obtained primarily through part of the European Nucleotide Archive (ENA) (2), and submissions from individual laboratories and batch the DNA Data Bank of Japan (DDBJ) (3) as a partner submissions from large-scale sequencing projects, in the International Nucleotide Sequence Database including whole-genome shotgun (WGS) and envir- Collaboration (INSDC). The INSDC partners exchange onmental sampling projects. Most submissions data daily to ensure that a uniform and comprehensive http://nar.oxfordjournals.org/ are made using the web-based BankIt or standalone collection of sequence information is available worldwide. Sequin programs, and accession numbers are NCBI makes the GenBank data available at no cost over the Internet, through FTP and a wide range of web-based assigned by GenBank staff upon receipt. Daily data retrieval and analysis services (4). -
Thesis : Genomic Regulation of Oestrous Behaviour in Dairy Cows
th a ommad K Arun s w o c y r i a in d Arun Kommadath 2012 Propositions 1. Quantitative trait associated gene expression analysis answers different questions than the classical differential expression analysis in microarray based studies (this thesis). 2. Communication between brain areas orchestrates sexual behaviour (this thesis). 3. In bioinformatics analyses, biological interpretation is more important than statistical significance. 4. The trend that technological advances in science outpace legal regulatory frameworks governing them should be reversed. 5. It is from our children that we fully realize what we mean to our parents. 6. In science as in life, what seemed the absolute truth yesterday can be refuted today, and what seems farfetched today can be conventional tomorrow. Propositions belonging to the thesis entitled, ‘Genomic regulation of oestrous behaviour in dairy cows’. Arun Kommadath Wageningen, 24th February 2012 Genomic regulation of oestrous behaviour in dairy cows Thesis committee Thesis supervisor Prof. dr. Mari A. Smits Personal chair at Animal Breeding and Genomics Centre Wageningen University Prof. dr. Martien A.M. Groenen Personal chair at Animal Breeding and Genomics Centre Wageningen University Thesis co-supervisors Dr. Marinus F.W. te Pas Senior Researcher at Animal Breeding and Genomics Centre Wageningen University Other members Prof. dr. Bas Kemp, Wageningen University Prof. dr. Jaap Keijer, Wageningen University Prof. dr. Dirk-Jan de Koning, Swedish University of Agricultural Sciences, Uppsala, Sweden Prof. dr. Eckhard Wolf, Ludwig-Maximilians University, Munich, Germany This research was conducted under the auspices of the Graduate School of Wageningen Institute of Animal Sciences (WIAS). Genomic regulation of oestrous behaviour in dairy cows Arun Kommadath Thesis submitted in fulfilment of the requirements for the degree of doctor at Wageningen University by the authority of the Rector Magnificus Prof.dr. -
Data Sheet 106
Rudolf-Wissell-Str. 28a Background 37079 Göttingen, Germany Phone: +49 551-50556-0 Synapsins are neuron-specific phosphoproteins that are exclusively associated with small synaptic Fax: +49 551-50556-384 vesicles, with little or no expression in other tissues including neuroendocrine cells. In mammals, three E-mail: [email protected] distinct synapsin genes (synapsin 1, 2, and 3) encode more than eight neuronal isoforms. Web: www.sysy.com Synapsin 1 is one of the most specific markers of synapses throughout the central and peripheral nervous system. In addition to synaptic nerve terminals, the protein is also present in certain sensory Synapsin 1/2 nerve endings. It is expressed in two splice variants (synapsin 1a and synapsin 1b). Synapsin 1 interacts Cat.No. 106 004; Polyclonal Guinea pig antibody, 100 µl antiserum (lyophilized) with vesicle membranes as well as with actin and spectrin. Synapsin 2 is expressed in the nervous system and also two splice variants were described so far, while synapsin 3 shows a more restricted expression pattern and is mainly found in the hypocampus. Data Sheet Synapsins are major phosphoproteins and are substrates for several protein kinases such as PKA, CaMK I and CaMK II. Synapsin 1 is widely used as reference substrate for calmodulin-dependent protein kinases. Reconstitution/ 100 µl antiserum, lyophilized. For reconstitution add 100 µl H2O, then aliquot and Storage store at -20°C until use. For detailed information, see back of the data sheet. Selected References for 106 004 Applications WB: 1 : 1000 (AP staining) IP: not tested yet An integrated transcriptomics and proteomics analysis reveals functional endocytic dysregulation caused by mutations in ICC: 1 : 1000 LRRK2. -
Rapid Evolution and Selection Inferred from the Transcriptomes of Sympatric Crater Lake Cichlid Fishes
Rapid evolution and selection inferred from the transcriptomes of sympatric crater lake cichlid fishes K. R. ELMER, S. FAN, H. M. GUNTER, J. C. JONES, S. BOEKHOFF, S. KURAKU and A. MEYER Lehrstuhl fUr Zoologie und Evolutionsbiologie, Department of Biology, University of Konstanz, Universitiitstrasse 10, 78457 Konstanz, Germany Abstract Crater lakes provide a natural laboratory to study speciation of cichlid fishes by ecological divergence. Up to now, there has been a dearth of transcriptomic and genomic information that would aid in understanding the molecular basis of the phenotypic differentiation between young species. We used next-generation sequencing (Roche 454 massively parallel pyrosequencing) to characterize the diversity of expressed sequence tags between ecologically divergent, endemic and sympatric species of cichlid fishes from crater lake Apoyo, Nicaragua: benthic Amphilophus astorquii and limnetic Amphilophus zaliosus. We obtained 24174 A. astorquii and 21382 A. zaliosus high quality expressed sequence tag contigs, of which 13 106 pairs are orthologous between species. Based on the ratio of non synonymous to synonymous substitutions, we identified six sequences exhibiting signals of strong diversifying selection (KalKs > 1). These included genes involved in biosynthesis, metabolic processes and development. This transcriptome sequence variation may be reflective of natural selection acting on the genomes of these young, sympatric sister species. Based on Ks ratios and p-distances between 3'-untranslated regions (UTRs) calibrated to previously published species divergence times, we estimated a neutral transcriptome-wide substitutional mutation rate of ~1.25 x 10-6 per site per year. We conclude that next-generation sequencing technologies allow us to infer natural selection acting to diversify the genomes of young species, such as crater lake cichlids, with much greater scope than previously possible. -
Identification of RNA Bound to the TDP-43 Ribonucleoprotein Complex in the Adult Mouse Brain
Identification of RNA bound to the TDP-43 ribonucleoprotein complex in the adult mouse brain Running Title: Identification of RNA bound to TDP-43 Ramesh K. Narayanan1, Marie Mangelsdorf1, Ajay Panwar1, Tim J. Butler1, Peter G. Noakes1,2, Robyn H. Wallace1,3* 1Queensland Brain Institute, 2School of Biomedical Sciences, 3School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, 4072, Australia *Corresponding author: [email protected] Objectives. Cytoplasmic inclusions containing TDP-43 are a pathological hallmark of several neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. TDP-43 is an RNA binding protein involved in gene regulation through control of RNA transcription, splicing and transport. However, the function of TDP-43 in the nervous system is largely unknown and its role in the pathogenesis of ALS is unclear. The aim of this study was to identify genes in the central nervous system that are regulated by TDP-43. Methods. RNA-immunoprecipitation with anti-TDP-43 antibody, followed by microarray analysis (RIP- chip), was used to isolate and identify RNA bound to TDP-43 protein from mouse brain. Results. This analysis produced a list of 1,839 potential TDP-43 gene targets, many of which overlap with previous studies and whose functions include RNA processing and synaptic function. Immunohistochemistry demonstrated that the TDP-43 protein could be found at the presynaptic membrane of axon terminals in the neuromuscular junction in mice. Conclusions. The finding that TDP-43 binds to RNA that codes for genes related to synaptic function, together with the localisation of TDP-43 protein at axon terminals, suggest a role for TDP-43 in the transport of synaptic mRNAs into distal processes. -
Comparative Expressed-Sequence-Tag Analysis of Differential Gene Expression Profiles in PC-12 Cells Before and After Nerve Growth Factor Treatment NORMAN H
Proc. Natl. Acad. Sci. USA Vol. 92, pp. 8303-8307, August 1995 Cell Biology Comparative expressed-sequence-tag analysis of differential gene expression profiles in PC-12 cells before and after nerve growth factor treatment NORMAN H. LEE, KEITH G. WEINSTOCK, EWEN F. KIRKNESS, JULIE A. EARLE-HUGHES, REBECCA A. FULDNER, SIMOS MARMAROS, ANNA GLODEK, JEANNINE D. GOCAYNE, MARK D. ADAMS, ANTHONY R. KERLAVAGE, CLAIRE M. FRASER, AND J. CRAIG VENTER The Institute for Genomic Research, 932 Clopper Road, Gaithersburg, MD 20878 Communicated by Martin Rodbell, National Institute of Environmental Health Sciences, Research Triangle Park NC, April 24, 1995 ABSTRACT Nerve growth factor-induced differentiation clones identified as differentially regulated by this approach of adrenal chromaffin PC-12 cells to a neuronal phenotype was confirmed by RNA blot analysis, thereby demonstrating involves alterations in gene expression and represents a model the potential of this technique in gene discovery and differ- system to study neuronal differentiation. We have used the ential gene expression.* expressed-sequence-tag approach to identify "600 differen- tially expressed mRNAs in untreated and nerve growth factor- treated PC-12 cells that encode proteins with diverse struc- EXPERIMENTAL PROCEDURES tural and biochemical functions. Many of these mRNAs en- cDNA Libraries. PC-12 cells (American Type Culture Col- code proteins belonging to cellular pathways not previously lection) were cultured and treated with 2.5S NGF (50 ng/ml) known to be regulated by nerve growth factor. Comparative as described (11). PC-12 cells undergo mitotic arrest and expressed-sequence-tag analysis provides a basis for survey- neuron-like phenotypic expression by day 7 of NGF treatment ing global changes in gene-expression patterns in response to (12); hence, cDNA libraries were constructed from untreated biological signals at an unprecedented scale, is a powerful tool PC-12 cells and PC-12 cells treated with NGF for 9 days. -
Genomic Approaches to Research in Lung Cancer Edward Gabrielson the Johns Hopkins University School of Medicine, Baltimore, USA
http://respiratory-research.com/content/1/1/036 Review Genomic approaches to research in lung cancer Edward Gabrielson The Johns Hopkins University School of Medicine, Baltimore, USA Received: 21 April 2000 Respir Res 2000, 1:36–39 Revisions requested: 11 May 2000 The electronic version of this article can be found online at Revisions received: 1 June 2000 http://respiratory-research.com/content/1/1/036 Accepted: 1 June 2000 Published: 23 June 2000 © Current Science Ltd (Print ISSN 1465-9921; Online ISSN 1465-993X) Abstract The medical research community is experiencing a marked increase in the amount of information available on genomic sequences and genes expressed by humans and other organisms. This information offers great opportunities for improving our understanding of complex diseases such as lung cancer. In particular, we should expect to witness a rapid increase in the rate of discovery of genes involved in lung cancer pathogenesis and we should be able to develop reliable molecular criteria for classifying lung cancers and predicting biological properties of individual tumors. Achieving these goals will require collaboration by scientists with specialized expertise in medicine, molecular biology, and decision-based statistical analysis. Keywords: cDNA arrays, genomics, lung cancer Introduction those diseases. Knowing the polymorphisms that make Genomics – the discipline that characterizes the struc- each of us unique individuals could be the key in the future tural and functional anatomy of the genome – has to predicting individual risks for developing disease and attracted continuously increased interest and invest- individual responses to pharmacological agents. However, ment over the past decade. The complete sequencing the full impact of genomics on medical research is still of the human genome is expected within a few years; unknown. -
Mechanisms of Α-Synuclein Induced Synaptopathy in Parkinson's Disease
King’s Research Portal DOI: 10.3389/fnins.2018.00080 Document Version Publisher's PDF, also known as Version of record Link to publication record in King's Research Portal Citation for published version (APA): Bridi, J. C., & Hirth, F. (2018). Mechanisms of -Synuclein Induced Synaptopathy in Parkinson's Disease. Frontiers in Neuroscience, 12, 80. https://doi.org/10.3389/fnins.2018.00080 Citing this paper Please note that where the full-text provided on King's Research Portal is the Author Accepted Manuscript or Post-Print version this may differ from the final Published version. If citing, it is advised that you check and use the publisher's definitive version for pagination, volume/issue, and date of publication details. And where the final published version is provided on the Research Portal, if citing you are again advised to check the publisher's website for any subsequent corrections. General rights Copyright and moral rights for the publications made accessible in the Research Portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognize and abide by the legal requirements associated with these rights. •Users may download and print one copy of any publication from the Research Portal for the purpose of private study or research. •You may not further distribute the material or use it for any profit-making activity or commercial gain •You may freely distribute the URL identifying the publication in the Research Portal Take down policy If you believe that this document breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim.