Proceedings of the International Workshop On
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Data Sheet 160-3P
Rudolf-Wissell-Str. 28a Background 37079 Göttingen, Germany Phone: +49 551-50556-0 Homer is a scaffolding protein of the post synaptic density (PSD) and enriched at excitatory synapses. Fax: +49 551-50556-384 The protein binds metabotropic glutamate receptors, TRPC1, proteins of the Shank family and others. E-mail: [email protected] By aggregating these proteins into clusters, Homer was suggested to organize distinct signalling Web: www.sysy.com domains. Homer 3 Three isoforms, Homer 1, 2 and 3 have been described. Each of these isoforms is subject to alternative splicing yielding the splice variants a, b, c, d. Cat.No. 160-3P; control protein, 100 µg protein (lyophilized) Data Sheet Selected General References Homer2 and Homer3 interact with amyloid precursor protein and inhibit Abeta production. Parisiadou L, Bethani I, Michaki V, Krousti K, Rapti G, Efthimiopoulos S Reconstitution/ 100 µg lyophilized protein. For reconstitution add 100 µl H2O to get a 1mg/ml Neurobiology of disease (2008) 303: 353-64. Storage solution in MBS. Then aliquot and store at -20°C until use. Differential expression of Homer family proteins in the developing mouse brain. For detailed information, see back of the data sheet. Shiraishi Y, Mizutani A, Yuasa S, Mikoshiba K, Furuichi T The Journal of comparative neurology (2004) 4734: 582-99. Immunogen Recombinant protein corresponding to AA 1 to 177 from rat Homer3 (UniProt Id: Q9Z2X5) Molecular characterisation of two structurally distinct groups of human homers, generated by extensive alternative splicing. Soloviev MM, Ciruela F, Chan WY, McIlhinney RA Recommended Optimal concentrations should be determined by the end-user. -
Mitotic Chromosome Binding Predicts Transcription Factor Properties in Interphase
bioRxiv preprint doi: https://doi.org/10.1101/404723; this version posted August 31, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Mitotic chromosome binding predicts transcription factor properties in interphase Authors: Mahé Raccaud1, Andrea B. Alber1,2, Elias T. Friman1,2, Harsha Agarwal3, Cédric Deluz1, Timo Kuhn3, J. Christof M. Gebhardt3 and David M. Suter1,4 Affiliations: 1Institute of Bioengineering, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, CH-1015, Switzerland 2These authors contributed equally 3Institute of Biophysics, Ulm University, Albert-Einstein-Allee 11, Ulm 89081, Germany 4Lead contact Corresponding author: David M. Suter ([email protected]) Summary Mammalian transcription factors (TFs) differ broadly in their nuclear mobility and sequence- specific/non-specific DNA binding affinity. How these properties affect the ability of TFs to occupy their specific binding sites in the genome and modify the epigenetic landscape is unclear. Here we combined live cell quantitative measurements of mitotic chromosome binding (MCB) of 502 TFs, measurements of TF mobility by fluorescence recovery after photobleaching, single molecule imaging of DNA binding in live cells, and genome-wide mapping of TF binding and chromatin accessibility. MCB scaled with interphase properties such as association with DNA-rich compartments, mobility, as well as large differences in genome-wide specific site occupancy that correlated with TF impact on chromatin accessibility. As MCB is largely mediated by electrostatic, non-specific TF-DNA interactions, our data suggests that non-specific DNA binding of TFs enhances their search for specific sites and thereby their impact on the accessible chromatin landscape. -
Scorpion Toxins Targeted Against the Sarcoplasmic Reticulum Ca2+-Release Channel of Skeletal and Cardiac Muscle
Proc. Nati. Acad. Sci. USA Vol. 89, pp. 12185-12189, December 1992 Physiology Scorpion toxins targeted against the sarcoplasmic reticulum Ca2+-release channel of skeletal and cardiac muscle (ryanodine receptors/Pandinus imperator venom/planar bilayer/ventricular myocytes/Ca2+ indicator) HECTOR H. VALDIVIA*t, MARK S. KIRBYf, W. JONATHAN LEDERER*, AND ROBERTO CORONADO*t *Department of Physiology, University of Wisconsin School of Medicine, Madison, WI 53706; and tDepartment of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201 Communicated by Michael V. L. Bennett, September 21, 1992 ABSTRACT We report the purification of two peptides, peratoxin inhibitor (IpTxi)] or activated [imperatoxin activa- called "imperatoxin inhibitor" and "imperatoxin activator," tor (IpTxa)] ryanodine receptors of skeletal and cardiac from the venom of the scorpion Pandinus imperator targeted muscle. Part of these results have been communicated in an against ryanodine receptor Ca2+-release channels. Impera- abstract form (8). toxin inhibitor has a Mr of 10,500, inhibits [3Hjryanodine binding to skeletal and cardiac sarcoplasmic reticulum with an EDso of 10 nM, and blocks openings of skeletal and cardiac EXPERIMENTAL PROCEDURES Ca2+-release channels incorporated into planar bilayers. In Purification of Scorpion Toxins. Lyophilized P. imperator whole-cell recordings of cardiac myocytes, imperatoxin inhib- venom was obtained from Latoxan (Rosans, France). Venom itor decreased twitch amplitude and intracellular Ca2+ tran- (50 mg per batch) was extracted in 2-3 ml of deionized water sients, suggesting a selective blockade of Ca2+ release from the and chromatographed on a column (1. 5 x 125 cm) of Sepha- sarcoplasmic reticulum. Imperatoxin activator has a Mr of dex G-50 fine. -
Multiple Actions of Φ-LITX-Lw1a on Ryanodine Receptors Reveal a Functional Link Between Scorpion DDH and ICK Toxins
Multiple actions of φ-LITX-Lw1a on ryanodine receptors reveal a functional link between scorpion DDH and ICK toxins Jennifer J. Smitha, Irina Vettera, Richard J. Lewisa, Steve Peigneurb, Jan Tytgatb, Alexander Lamc, Esther M. Gallantc, Nicole A. Beardd, Paul F. Alewooda,1,2, and Angela F. Dulhuntyc,1,2 aChemical and Structural Biology, Institute for Molecular Biosciences, University of Queensland, St. Lucia, QLD 4072, Australia; bLaboratory of Toxicology, University of Leuven, 3000 Leuven, Belgium; cDepartment of Molecular Bioscience, John Curtin School of Medical Research, Australian National University, Canberra, ACT 2601, Australia; and dDiscipline of Biomedical Sciences, Faculty of Education, Science, Technology and Mathematics, University of Canberra, Canberra, ACT 2601, Australia Edited by Clara Franzini-Armstrong, University of Pennsylvania Medical Center, Philadelphia, PA, and approved April 23, 2013 (received for review August 26, 2012) We recently reported the isolation of a scorpion toxin named U1- mutations, atypical posttranslational modifications of RyRs, liotoxin-Lw1a (U1-LITX-Lw1a) that adopts an unusual 3D fold termed including hyperphosphorylation and S-nitrosylation, have been the disulfide-directed hairpin (DDH) motif, which is the proposed implicated in heart failure and pathologic muscle fatigue (10– evolutionary structural precursor of the three-disulfide-containing 12). Because of their wide distribution, there is mounting evidence inhibitor cystine knot (ICK) motif found widely in animals and plants. to suggest that dysregulation of RyRs also plays a role in a plethora Here we reveal that U1-LITX-Lw1a targets and activates the mam- of other disease states, including chronic pain, neurodegenerative malian ryanodine receptor intracellular calcium release channel (RyR) disorders such as Alzheimer’s disease, and intellectual deficit (13– with high (fM) potency and provides a functional link between DDH 15). -
Maurocalcine-Derivatives As Biotechnological Tools for The
Maurocalcine-derivatives as biotechnological tools for the penetration of cell-impermeable compounds Narendra Ram, Emilie Jaumain, Michel Ronjat, Fabienne Pirollet, Michel de Waard To cite this version: Narendra Ram, Emilie Jaumain, Michel Ronjat, Fabienne Pirollet, Michel de Waard. Maurocalcine- derivatives as biotechnological tools for the penetration of cell-impermeable compounds: Technological value of a scorpion toxin. de Lima, M.E.; de Castro Pimenta, A.M.; Martin-Eauclaire, M.F.; Bendeta Zengali, R.; Rochat, H. E. Animal Toxins: state of the art: Perspectives in Health and Biotechnology., Editora UFMG Belo Horizonte, Brazil, pp.715-732, 2009. inserm-00515224 HAL Id: inserm-00515224 https://www.hal.inserm.fr/inserm-00515224 Submitted on 5 Sep 2013 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Maurocalcine-derivatives as biotechnological tools for the penetration of cell-impermeable compounds by Narendra Ram1,2, Emilie Jaumain1,2, Michel Ronjat1,2, Fabienne Pirollet1,2 & Michel De Waard1,2* 1 INSERM, U836, Team 3: Calcium channels, functions and pathologies, BP 170, Grenoble Cedex 9, F-38042, France 2 Université Joseph Fourier, Institut des Neurosciences, BP 170, Grenoble Cedex 9, F-38042, France Running title: Technological value of a scorpion toxin *To whom correspondence should be sent: Dr. -
Multivariate Analysis Reveals Genetic Associations of the Resting Default
Multivariate analysis reveals genetic associations of PNAS PLUS the resting default mode network in psychotic bipolar disorder and schizophrenia Shashwath A. Medaa,1, Gualberto Ruañob,c, Andreas Windemuthb, Kasey O’Neila, Clifton Berwisea, Sabra M. Dunna, Leah E. Boccaccioa, Balaji Narayanana, Mohan Kocherlab, Emma Sprootena, Matcheri S. Keshavand, Carol A. Tammingae, John A. Sweeneye, Brett A. Clementzf, Vince D. Calhoung,h,i, and Godfrey D. Pearlsona,h,j aOlin Neuropsychiatry Research Center, Institute of Living at Hartford Hospital, Hartford, CT 06102; bGenomas Inc., Hartford, CT 06102; cGenetics Research Center, Hartford Hospital, Hartford, CT 06102; dDepartment of Psychiatry, Beth Israel Deaconess Hospital, Harvard Medical School, Boston, MA 02215; eDepartment of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX 75390; fDepartment of Psychology, University of Georgia, Athens, GA 30602; gThe Mind Research Network, Albuquerque, NM 87106; Departments of hPsychiatry and jNeurobiology, Yale University, New Haven, CT 06520; and iDepartment of Electrical and Computer Engineering, The University of New Mexico, Albuquerque, NM 87106 Edited by Robert Desimone, Massachusetts Institute of Technology, Cambridge, MA, and approved April 4, 2014 (received for review July 15, 2013) The brain’s default mode network (DMN) is highly heritable and is Although risk for psychotic illnesses is driven in small part by compromised in a variety of psychiatric disorders. However, ge- highly penetrant, often private mutations such as copy number netic control over the DMN in schizophrenia (SZ) and psychotic variants, substantial risk also is likely conferred by multiple genes bipolar disorder (PBP) is largely unknown. Study subjects (n = of small effect sizes interacting together (7). According to the 1,305) underwent a resting-state functional MRI scan and were “common disease common variant” (CDCV) model, one would analyzed by a two-stage approach. -
Statistical and Bioinformatic Analysis of Hemimethylation Patterns in Non-Small Cell Lung Cancer
Statistical and Bioinformatic Analysis of Hemimethylation Patterns in Non-Small Cell Lung Cancer Shuying Sun ( [email protected] ) Texas State University San Marcos https://orcid.org/0000-0003-3974-6996 Austin Zane Texas A&M University College Station Carolyn Fulton Schreiner University Jasmine Philipoom Case Western Reserve University Research article Keywords: Methylation, Hemimethylation, Lung Cancer, Bioinformatics, Epigenetics Posted Date: October 12th, 2020 DOI: https://doi.org/10.21203/rs.3.rs-17794/v2 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Version of Record: A version of this preprint was published on March 12th, 2021. See the published version at https://doi.org/10.1186/s12885-021-07990-7. Page 1/29 Abstract Background: DNA methylation is an epigenetic event involving the addition of a methyl-group to a cytosine-guanine base pair (i.e., CpG site). It is associated with different cancers. Our research focuses on studying non- small cell lung cancer hemimethylation, which refers to methylation occurring on only one of the two DNA strands. Many studies often assume that methylation occurs on both DNA strands at a CpG site. However, recent publications show the existence of hemimethylation and its signicant impact. Therefore, it is important to identify cancer hemimethylation patterns. Methods: In this paper, we use the Wilcoxon signed rank test to identify hemimethylated CpG sites based on publicly available non-small cell lung cancer methylation sequencing data. We then identify two types of hemimethylated CpG clusters, regular and polarity clusters, and genes with large numbers of hemimethylated sites. -
Venom Week 2012 4Th International Scientific Symposium on All Things Venomous
17th World Congress of the International Society on Toxinology Animal, Plant and Microbial Toxins & Venom Week 2012 4th International Scientific Symposium on All Things Venomous Honolulu, Hawaii, USA, July 8 – 13, 2012 1 Table of Contents Section Page Introduction 01 Scientific Organizing Committee 02 Local Organizing Committee / Sponsors / Co-Chairs 02 Welcome Messages 04 Governor’s Proclamation 08 Meeting Program 10 Sunday 13 Monday 15 Tuesday 20 Wednesday 26 Thursday 30 Friday 36 Poster Session I 41 Poster Session II 47 Supplemental program material 54 Additional Abstracts (#298 – #344) 61 International Society on Thrombosis & Haemostasis 99 2 Introduction Welcome to the 17th World Congress of the International Society on Toxinology (IST), held jointly with Venom Week 2012, 4th International Scientific Symposium on All Things Venomous, in Honolulu, Hawaii, USA, July 8 – 13, 2012. This is a supplement to the special issue of Toxicon. It contains the abstracts that were submitted too late for inclusion there, as well as a complete program agenda of the meeting, as well as other materials. At the time of this printing, we had 344 scientific abstracts scheduled for presentation and over 300 attendees from all over the planet. The World Congress of IST is held every three years, most recently in Recife, Brazil in March 2009. The IST World Congress is the primary international meeting bringing together scientists and physicians from around the world to discuss the most recent advances in the structure and function of natural toxins occurring in venomous animals, plants, or microorganisms, in medical, public health, and policy approaches to prevent or treat envenomations, and in the development of new toxin-derived drugs. -
Supplementary Materials
Supplementary materials Supplementary Table S1: MGNC compound library Ingredien Molecule Caco- Mol ID MW AlogP OB (%) BBB DL FASA- HL t Name Name 2 shengdi MOL012254 campesterol 400.8 7.63 37.58 1.34 0.98 0.7 0.21 20.2 shengdi MOL000519 coniferin 314.4 3.16 31.11 0.42 -0.2 0.3 0.27 74.6 beta- shengdi MOL000359 414.8 8.08 36.91 1.32 0.99 0.8 0.23 20.2 sitosterol pachymic shengdi MOL000289 528.9 6.54 33.63 0.1 -0.6 0.8 0 9.27 acid Poricoic acid shengdi MOL000291 484.7 5.64 30.52 -0.08 -0.9 0.8 0 8.67 B Chrysanthem shengdi MOL004492 585 8.24 38.72 0.51 -1 0.6 0.3 17.5 axanthin 20- shengdi MOL011455 Hexadecano 418.6 1.91 32.7 -0.24 -0.4 0.7 0.29 104 ylingenol huanglian MOL001454 berberine 336.4 3.45 36.86 1.24 0.57 0.8 0.19 6.57 huanglian MOL013352 Obacunone 454.6 2.68 43.29 0.01 -0.4 0.8 0.31 -13 huanglian MOL002894 berberrubine 322.4 3.2 35.74 1.07 0.17 0.7 0.24 6.46 huanglian MOL002897 epiberberine 336.4 3.45 43.09 1.17 0.4 0.8 0.19 6.1 huanglian MOL002903 (R)-Canadine 339.4 3.4 55.37 1.04 0.57 0.8 0.2 6.41 huanglian MOL002904 Berlambine 351.4 2.49 36.68 0.97 0.17 0.8 0.28 7.33 Corchorosid huanglian MOL002907 404.6 1.34 105 -0.91 -1.3 0.8 0.29 6.68 e A_qt Magnogrand huanglian MOL000622 266.4 1.18 63.71 0.02 -0.2 0.2 0.3 3.17 iolide huanglian MOL000762 Palmidin A 510.5 4.52 35.36 -0.38 -1.5 0.7 0.39 33.2 huanglian MOL000785 palmatine 352.4 3.65 64.6 1.33 0.37 0.7 0.13 2.25 huanglian MOL000098 quercetin 302.3 1.5 46.43 0.05 -0.8 0.3 0.38 14.4 huanglian MOL001458 coptisine 320.3 3.25 30.67 1.21 0.32 0.9 0.26 9.33 huanglian MOL002668 Worenine -
Adrenaline Stimulates Glucagon Secretion by Tpc2-Dependent
1128 Diabetes Volume 67, June 2018 Adrenaline Stimulates Glucagon Secretion by Tpc2- Dependent Ca2+ Mobilization From Acidic Stores in Pancreatic a-Cells Alexander Hamilton,1 Quan Zhang,1 Albert Salehi,2 Mara Willems,1 Jakob G. Knudsen,1 Anna K. Ringgaard,3,4 Caroline E. Chapman,1 Alejandro Gonzalez-Alvarez,1 Nicoletta C. Surdo,5 Manuela Zaccolo,5 Davide Basco,6 Paul R.V. Johnson,1,7 Reshma Ramracheya,1 Guy A. Rutter,8 Antony Galione,9 Patrik Rorsman,1,2,7 and Andrei I. Tarasov1,7 Diabetes 2018;67:1128–1139 | https://doi.org/10.2337/db17-1102 Adrenaline is a powerful stimulus of glucagon secretion. It The ability of the “fight-or-flight” hormone adrenaline to acts by activation of b-adrenergic receptors, but the down- increase plasma glucose levels by stimulating liver gluconeo- stream mechanisms have only been partially elucidated. genesis is in part mediated by glucagon, the body’sprincipal Here, we have examined the effects of adrenaline in mouse hyperglycemic hormone (1). Glucagon is secreted by the and human a-cells by a combination of electrophysiology, a-cells of the pancreas (2). Reduced autonomic stimulation 2+ imaging of Ca and PKA activity, and hormone release of glucagon secretion may result in hypoglycemia, a serious measurements. We found that stimulation of glucagon and potentially fatal complication of diabetes (3). It has been secretion correlated with a PKA- and EPAC2-dependent estimated that up to 10% of insulin-treated patients die of (inhibited by PKI and ESI-05, respectively) elevation of hypoglycemia (4). Understanding the mechanism by which [Ca2+] in a-cells, which occurred without stimulation of i adrenaline stimulates glucagon secretion and how it becomes ISLET STUDIES electrical activity and persisted in the absence of extracel- perturbed in patients with diabetes is therefore essential. -
Brain Region-Dependent Gene Networks Associated with Selective Breeding for Increased Voluntary Wheel-Running Behavior
UC Riverside UC Riverside Previously Published Works Title Brain region-dependent gene networks associated with selective breeding for increased voluntary wheel-running behavior. Permalink https://escholarship.org/uc/item/8c49g8fd Journal PloS one, 13(8) ISSN 1932-6203 Authors Zhang, Pan Rhodes, Justin S Garland, Theodore et al. Publication Date 2018 DOI 10.1371/journal.pone.0201773 Peer reviewed eScholarship.org Powered by the California Digital Library University of California RESEARCH ARTICLE Brain region-dependent gene networks associated with selective breeding for increased voluntary wheel-running behavior Pan Zhang1,2, Justin S. Rhodes3,4, Theodore Garland, Jr.5, Sam D. Perez3, Bruce R. Southey2, Sandra L. Rodriguez-Zas2,6,7* 1 Illinois Informatics Institute, University of Illinois at Urbana-Champaign, Urbana, IL, United States of America, 2 Department of Animal Sciences, University of Illinois at Urbana-Champaign, Urbana, IL, United a1111111111 States of America, 3 Beckman Institute for Advanced Science and Technology, Urbana, IL, United States of a1111111111 America, 4 Center for Nutrition, Learning and Memory, University of Illinois at Urbana-Champaign, Urbana, a1111111111 IL, United States of America, 5 Department of Evolution, Ecology, and Organismal Biology, University of a1111111111 California, Riverside, CA, United States of America, 6 Department of Statistics, University of Illinois at Urbana-Champaign, Urbana, IL, United States of America, 7 Carle Woese Institute for Genomic Biology, a1111111111 University of Illinois at Urbana-Champaign, Urbana, IL, United States of America * [email protected] OPEN ACCESS Abstract Citation: Zhang P, Rhodes JS, Garland T, Jr., Perez SD, Southey BR, Rodriguez-Zas SL (2018) Brain Mouse lines selectively bred for high voluntary wheel-running behavior are helpful models region-dependent gene networks associated with for uncovering gene networks associated with increased motivation for physical activity and selective breeding for increased voluntary wheel- other reward-dependent behaviors. -
HOMER2 (NM 199330) Human Tagged ORF Clone – RC223154L4
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for RC223154L4 HOMER2 (NM_199330) Human Tagged ORF Clone Product data: Product Type: Expression Plasmids Product Name: HOMER2 (NM_199330) Human Tagged ORF Clone Tag: mGFP Symbol: HOMER2 Synonyms: ACPD; CPD; DFNA68; HOMER-2; VESL-2 Vector: pLenti-C-mGFP-P2A-Puro (PS100093) E. coli Selection: Chloramphenicol (34 ug/mL) Cell Selection: Puromycin ORF Nucleotide The ORF insert of this clone is exactly the same as(RC223154). Sequence: Restriction Sites: SgfI-MluI Cloning Scheme: ACCN: NM_199330 ORF Size: 1062 bp This product is to be used for laboratory only. Not for diagnostic or therapeutic use. View online » ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 1 / 2 HOMER2 (NM_199330) Human Tagged ORF Clone – RC223154L4 OTI Disclaimer: The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info OTI Annotation: This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene. RefSeq: NM_199330.1 RefSeq Size: 2005 bp RefSeq ORF: 1065 bp Locus ID: 9455 UniProt ID: Q9NSB8 Protein Families: Druggable Genome MW: 40.4 kDa Gene Summary: This gene encodes a member of the homer family of dendritic proteins.