SEPT4 Blocking Peptide (CDBP5105) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use

Total Page：16

File Type：pdf, Size：1020Kb

SEPT4 blocking peptide (CDBP5105) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Antigen Description This gene is a member of the septin family of nucleotide binding proteins, originally described in yeast as cell division cycle regulatory proteins. Septins are highly conserved in yeast, Drosophila, and mouse, and appear to regulate cytoskeletal organization. Disruption of septin function disturbs cytokinesis and results in large multinucleate or polyploid cells. This gene is highly expressed in brain and heart. Alternatively spliced transcript variants encoding different isoforms have been described for this gene. One of the isoforms (known as ARTS) is distinct; it is localized to the mitochondria, and has a role in apoptosis and cancer. [provided by RefSeq, Nov 2010] Immunogen 12 amino amino terminus of human ARTS. Nature Synthetic Expression System N/A Species Reactivity Human Conjugate Unconjugated Applications Used as a blocking peptide in immunoblotting applications. Procedure None Format Liquid Concentration 200 μg/mL Size 0.05mg Preservative None Storage -20°C ANTIGEN GENE INFORMATION Gene Name SEPT4 septin 4 [ Homo sapiens (human) ] Official Symbol SEPT4 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 1 © Creative Diagnostics All Rights Reserved Synonyms SEPT4; septin 4; H5; ARTS; MART; SEP4; CE5B3; PNUTL2; hucep-7; BRADEION; hCDCREL- 2; septin-4; septin-M; CE5B3 beta; bradeion beta; brain protein H5; cerebral protein 7; peanut- like protein 2; cell division control-related protein 2; apoptosis-related protein in the TGF-beta signaling pathway Entrez Gene ID 5414 mRNA Refseq NM_001198713 Protein Refseq NP_001185642 UniProt ID O43236 Pathway Apoptosis Modulation and Signaling Function GTP binding; GTPase activity; protein binding; structural molecule activity 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 2 © Creative Diagnostics All Rights Reserved.

Copy Link

Recommended publications

FK506-Binding Protein 12.6/1B, a Negative Regulator of [Ca2+], Rescues Memory and Restores Genomic Regulation in the Hippocampus of Aging Rats
This Accepted Manuscript has not been copyedited and formatted. The final version may differ from this version. A link to any extended data will be provided when the final version is posted online. Research Articles: Neurobiology of Disease FK506-Binding Protein 12.6/1b, a negative regulator of [Ca2+], rescues memory and restores genomic regulation in the hippocampus of aging rats John C. Gant1, Eric M. Blalock1, Kuey-Chu Chen1, Inga Kadish2, Olivier Thibault1, Nada M. Porter1 and Philip W. Landfield1 1Department of Pharmacology & Nutritional Sciences, University of Kentucky, Lexington, KY 40536 2Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294 DOI: 10.1523/JNEUROSCI.2234-17.2017 Received: 7 August 2017 Revised: 10 October 2017 Accepted: 24 November 2017 Published: 18 December 2017 Author contributions: J.C.G. and P.W.L. designed research; J.C.G., E.M.B., K.-c.C., and I.K. performed research; J.C.G., E.M.B., K.-c.C., I.K., and P.W.L. analyzed data; J.C.G., E.M.B., O.T., N.M.P., and P.W.L. wrote the paper. Conflict of Interest: The authors declare no competing financial interests. NIH grants AG004542, AG033649, AG052050, AG037868 and McAlpine Foundation for Neuroscience Research Corresponding author: Philip W. Landfield, [email protected], Department of Pharmacology & Nutritional Sciences, University of Kentucky, 800 Rose Street, UKMC MS 307, Lexington, KY 40536 Cite as: J. Neurosci ; 10.1523/JNEUROSCI.2234-17.2017 Alerts: Sign up at www.jneurosci.org/cgi/alerts to receive customized email alerts when the fully formatted version of this article is published.
[Show full text]
Cell Type-Specific Gene Expression Patterns Associated with Posttraumatic Stress Disorder in World Trade Center Responders
Kuan et al. Translational Psychiatry (2019) 9:1 https://doi.org/10.1038/s41398-018-0355-8 Translational Psychiatry ARTICLE Open Access Cell type-specific gene expression patterns associated with posttraumatic stress disorder in World Trade Center responders Pei-Fen Kuan1, Xiaohua Yang2,SeanClouston 3,XuRen1,RomanKotov4, Monika Waszczuk4,PrashantK.Singh5, Sean T. Glenn5, Eduardo Cortes Gomez 6, Jianmin Wang6,EvelynBromet4 and Benjamin J. Luft2 Abstract Posttraumatic stress disorder (PTSD), a chronic disorder resulting from severe trauma, has been linked to immunologic dysregulation. Gene expression profiling has emerged as a promising tool for understanding the pathophysiology of PTSD. However, to date, all but one gene expression study was based on whole blood or unsorted peripheral blood mononuclear cell (PBMC), a complex tissue consisting of several populations of cells. The objective of this study was to utilize RNA sequencing to simultaneously profile the gene expression of four immune cell subpopulations (CD4T, CD8T, B cells, and monocytes) in 39 World Trade Center responders (20 with and 19 without PTSD) to determine which immune subsets play a role in the transcriptomic changes found in whole blood. Transcriptome-wide analyses identified cell-specific and shared differentially expressed genes across the four cell types. FKBP5 and PI4KAP1 genes were consistently upregulated across all cell types. Notably, REST and SEPT4, genes linked to neurodegeneration, were among the top differentially expressed genes in monocytes. Pathway analyses identified differentially expressed gene sets involved in mast cell activation and regulation in CD4T, interferon-beta production in CD8T, and neutrophil- fi 1234567890():,; 1234567890():,; 1234567890():,; 1234567890():,; related gene sets in monocytes.
[Show full text]
Protein Kinase A-Mediated Septin7 Phosphorylation Disrupts Septin Filaments and Ciliogenesis
cells Article Protein Kinase A-Mediated Septin7 Phosphorylation Disrupts Septin Filaments and Ciliogenesis Han-Yu Wang 1,2, Chun-Hsiang Lin 1, Yi-Ru Shen 1, Ting-Yu Chen 2,3, Chia-Yih Wang 2,3,* and Pao-Lin Kuo 1,2,4,* 1 Department of Obstetrics and Gynecology, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan; [email protected] (H.-Y.W.); [email protected] (C.-H.L.); [email protected] (Y.-R.S.) 2 Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan; [email protected] 3 Department of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan 4 Department of Obstetrics and Gynecology, National Cheng-Kung University Hospital, Tainan 704, Taiwan * Correspondence: [email protected] (C.-Y.W.); [email protected] (P.-L.K.); Tel.: +886-6-2353535 (ext. 5338); (C.-Y.W.)+886-6-2353535 (ext. 5262) (P.-L.K.) Abstract: Septins are GTP-binding proteins that form heteromeric filaments for proper cell growth and migration. Among the septins, septin7 (SEPT7) is an important component of all septin filaments. Here we show that protein kinase A (PKA) phosphorylates SEPT7 at Thr197, thus disrupting septin filament dynamics and ciliogenesis. The Thr197 residue of SEPT7, a PKA phosphorylating site, was conserved among different species. Treatment with cAMP or overexpression of PKA catalytic subunit (PKACA2) induced SEPT7 phosphorylation, followed by disruption of septin filament formation. Constitutive phosphorylation of SEPT7 at Thr197 reduced SEPT7-SEPT7 interaction, but did not affect SEPT7-SEPT6-SEPT2 or SEPT4 interaction.
[Show full text]
Background Methods Conclusions Results
Gene Expression Profiles of Pediatric Tuberculosis Patients and Exposed Controls from India Jeffrey A Tornheim,1 Mandar Paradkar,2 Anil Madugundu,4,5 Nikhil Gupte,2 Vandana Kulkarni,2 Sreelakshmi Sreenivasamurthy,4,5 Remya Raja,4 Neeta Pradhan,2 Shri Vijay Bala Yogendra Shivakumar,6 Chhaya Valvi,3 Rewa Kohli,2 Padmapriyadarsini Chandrasekaran,7 Vidya Mave,2 Akhilesh Pandey,4,5 and Amita Gupta1 1Center for Clinical Global Health Education, Division of Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, MD, USA, 2Byramjee Jeejeebhoy Government Medical College – Johns Hopkins University Clinical Research Site, Pune, Maharashtra, India, 3Byramjee Jeejeebhoy Government Medical College, Pune, Maharashtra, India, 4National Institute of Mental Health and Neurosciences - Institute of Bioinformatics Lab, Bangalore, India, 5Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA, 6Johns Hopkins University – India office (CCGHE), Pune, Maharashtra, India, 7National Institute for Research in Tuberculosis, Chennai, Tamil Nadu, India BACKGROUND RESULTS—Differential Gene Expression Tuberculosis (TB) is the #1 infectious disease killer worldwide, and 27% of cases are in India (WHO 2016). Aim 1: Differential gene expression between pediatric cases (N=16) and controls (N=32) at enrollment Children frequently have either paucibacillary disease, are too young to provide adequate sputum Gene Counts Fold Change Distribution samples, or develop extrapulmonary disease, forcing clinicians to rely on diagnostic tests with poor sensitivity and frequent presumptive treatment for TB in children (Perez-Velez NEJM 2012). Several studies have attempted to use biomarkers of host response to infection as an alternative means of Number of Differentially Expressed Genes between Cases and Controls, diagnosing TB, but these studies have not included many children, Indian patients, or microbiologically by False Discovery Rate (FDR) and Log2-Fold Change Any Log2 >0.5 Log2 >1.0 Log2 >1.5 Log2 >2.0 confirmed patients.
[Show full text]
Gene Expression in the Mouse Eye: an Online Resource for Genetics Using 103 Strains of Mice
Molecular Vision 2009; 15:1730-1763 <http://www.molvis.org/molvis/v15/a185> © 2009 Molecular Vision Received 3 September 2008 | Accepted 25 August 2009 | Published 31 August 2009 Gene expression in the mouse eye: an online resource for genetics using 103 strains of mice Eldon E. Geisert,1 Lu Lu,2 Natalie E. Freeman-Anderson,1 Justin P. Templeton,1 Mohamed Nassr,1 Xusheng Wang,2 Weikuan Gu,3 Yan Jiao,3 Robert W. Williams2 (First two authors contributed equally to this work) 1Department of Ophthalmology and Center for Vision Research, Memphis, TN; 2Department of Anatomy and Neurobiology and Center for Integrative and Translational Genomics, Memphis, TN; 3Department of Orthopedics, University of Tennessee Health Science Center, Memphis, TN Purpose: Individual differences in patterns of gene expression account for much of the diversity of ocular phenotypes and variation in disease risk. We examined the causes of expression differences, and in their linkage to sequence variants, functional differences, and ocular pathophysiology. Methods: mRNAs from young adult eyes were hybridized to oligomer microarrays (Affymetrix M430v2). Data were embedded in GeneNetwork with millions of single nucleotide polymorphisms, custom array annotation, and information on complementary cellular, functional, and behavioral traits. The data include male and female samples from 28 common strains, 68 BXD recombinant inbred lines, as well as several mutants and knockouts. Results: We provide a fully integrated resource to map, graph, analyze, and test causes and correlations of differences in gene expression in the eye. Covariance in mRNA expression can be used to infer gene function, extract signatures for different cells or tissues, to define molecular networks, and to map quantitative trait loci that produce expression differences.
[Show full text]
UC San Diego UC San Diego Electronic Theses and Dissertations
UC San Diego UC San Diego Electronic Theses and Dissertations Title Astrocyte activity modulated by S1P-signaling in a multiple sclerosis model Permalink https://escholarship.org/uc/item/2bn557vr Author Groves, Aran Publication Date 2015 Peer reviewed|Thesis/dissertation eScholarship.org Powered by the California Digital Library University of California UNIVERSITY OF CALIFORNIA, SAN DIEGO Astrocyte activity modulated by S1P-signaling in a multiple sclerosis model A dissertation submitted in partial satisfaction of the requirements for the degree Doctor of Philosophy in Neurosciences by Aran Groves Committee in charge: Professor Jerold Chun, Chair Professor JoAnn Trejo, Co-Chair Professor Jody Corey-Bloom Professor Mark Mayford Professor William Mobley 2015 The Dissertation of Aran Groves is approved, and it is acceptable in quality and form for publication on microfilm and electronically: Co-Chair Chair University of California, San Diego 2015 iii TABLE OF CONTENTS Signature Page ..................................................................................................... iii Table of Contents ................................................................................................. iv List of Figures ....................................................................................................... vi List of Tables ....................................................................................................... viii Acknowledgments ................................................................................................
[Show full text]
Human SEPT4 Blocking Peptide (DAG-P0110) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use
Human SEPT4 blocking peptide (DAG-P0110) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Antigen Description This gene is a member of the septin family of nucleotide binding proteins, originally described in yeast as cell division cycle regulatory proteins. Septins are highly conserved in yeast, Drosophila, and mouse, and appear to regulate cytoskeletal organization. Disruption of septin function disturbs cytokinesis and results in large multinucleate or polyploid cells. This gene is highly expressed in brain and heart. Alternatively spliced transcript variants encoding different isoforms have been described for this gene. One of the isoforms (known as ARTS) is distinct; it is localized to the mitochondria, and has a role in apoptosis and cancer. [provided by RefSeq, Nov 2010] Specificity Widely expressed in adult and fetal tissues with highest expression in adult brain (at protein level), heart, liver and adrenal gland and fetal heart, kidney, liver and lung. Also expressed in colorectal cancers and malignant melanomas. Expressed in plate Nature Synthetic Expression System N/A Conjugate Unconjugated Applications BL Sequence Similarities Belongs to the septin family. Cellular Localization Cytoplasm. Cytoplasm > cytoskeleton. In platelets, found in areas surrounding alpha-granules and Mitochondrion. Nucleus. While predominantly localized in the mitochondria under resting conditions, isoform ARTS translocates into the nucleus after TGF-be Procedure None Format Liquid Buffer PBS with 0.1%
[Show full text]
SEPT2 Is a New Fusion Partner of MLL in Acute Myeloid Leukemia with T (2
Oncogene (2006) 25, 6147–6152 & 2006 Nature Publishing Group All rights reserved 0950-9232/06 $30.00 www.nature.com/onc ONCOGENOMICS SEPT2 is a new fusion partner of MLL in acute myeloid leukemia with t(2;11)(q37;q23) N Cerveira1, C Correia1, S Bizarro1, C Pinto1, S Lisboa1, JM Mariz2, M Marques2 and MR Teixeira1 1Department of Genetics, Portuguese Oncology Institute, Porto, Portugal and 2Department of Onco-Hematology, Portuguese Oncology Institute, Porto, Portugal We have identiﬁed a new mixed lineage leukemia (MLL) hematopoietic stem cells or progenitors (Daser and gene fusion partner in a patient with treatment-related Rabbitts, 2005; Li et al., 2005; Slany, 2005). Normally, acute myeloid leukemia (AML)presenting a HOX expression is high in hematopoietic stem cells and t(2;11)(q37;q23) as the only cytogenetic abnormality. becomes gradually extinguished during differentiation Fluorescence in situ hybridization demonstrated a re- (Grier et al., 2005). A failure to downregulate HOX arrangement of the MLL gene and molecular genetic expression inhibits hematopoietic maturation and can analyses identiﬁed a septin family gene, SEPT2, located lead to leukemia (Grier et al., 2005). on chromosome 2q37, as the fusion partner of MLL.RNA Abnormalities of 11q23 involving the MLL gene are and DNA analyses showed the existence of an in-frame found in several hematological malignancies, including fusion of MLL exon 7 with SEPT2 exon 3, with the acute lymphoblastic leukemia (ALL)and acute myeloid genomic breakpoints located in intron 7 and 2 of MLL leukemia (AML)(Huret, 2005).The overall incidence of and SEPT2, respectively. Search for DNA sequence MLL-associated leukemia is around 3 and 8–10% for motifs revealed the existence of two sequences with AML and ALL, respectively (Daser and Rabbitts, 94.4% homology with the topoisomerase II consensus 2005).
[Show full text]
(12) United States Patent (10) Patent No.: US 9,636,380 B2 Lammel Et Al
USOO963638 OB2 (12) United States Patent (10) Patent No.: US 9,636,380 B2 Lammel et al. (45) Date of Patent: May 2, 2017 (54) OPTOGENETIC CONTROL OF INPUTS TO 5,041,224 A 8/1991 Ohyama et al. THE VENTRAL TEGMENTAL AREA 5,082,670 A 1/1992 Gage et al. 5,249,575 A 10, 1993 Di Mino et al. 5,267,152 A 11/1993 Yang et al. (71) Applicant: The Board of Trustees of the Leland 5,290,280 A 3/1994 Daikuzono et al. Stanford Junior University, Palo Alto, 5.330,515 A 7, 1994 Rutecki et al. CA (US) 5,382,516 A 1, 1995 Bush 5,411,540 A 5, 1995 Edell et al. 5,445,608 A 8, 1995 Chen et al. (72) Inventors: Stephan Lammel, Stanford, CA (US); 5,460.950 A 10, 1995 Barr et al. Byungkook Lim, La Jolla, CA (US); 5,460.954 A 10, 1995 Lee et al. Robert C. Malenka, Palo Alto, CA 5,470,307 A 11/1995 Lindall (US) 5,495,541 A 2/1996 Murray et al. 5,520,188 A 5/1996 Hennige et al. 5,527,695 A 6/1996 Hodges et al. (73) Assignee: The Board of Trustees of the Leland 5,550,316 A 8, 1996 Mintz Stanford Junior University, Stanford, 5,641,650 A 6/1997 Turner et al. CA (US) 5,703.985 A 12/1997 Owyang et al. 5,722,426 A 3, 1998 Kolff (*) Notice: Subject to any disclaimer, the term of this 5,738,625 A 4/1998 Gluck patent is extended or adjusted under 35 5,739,273 A 4/1998 Engelman et al.
[Show full text]
Phenotype Characterisation of TBX4 Mutation and Deletion Carriers with Neonatal and Paediatric Pulmonary Hypertension
ORIGINAL ARTICLE PULMONARY HYPERTENSION AND PAEDIATRICS Phenotype characterisation of TBX4 mutation and deletion carriers with neonatal and paediatric pulmonary hypertension Csaba Galambos 1,19, Mary P. Mullen2,19, Joseph T. Shieh3, Nicolaus Schwerk4, Matthew J. Kielt5, Nicola Ullmann6, Renata Boldrini7, Irena Stucin-Gantar8, Cristina Haass9, Manish Bansal10, Pankaj B. Agrawal11, Joyce Johnson12, Donatella Peca7, Cecilia Surace7, Renato Cutrera 6, Michael W. Pauciulo13, William C. Nichols13, Matthias Griese14, Dunbar Ivy15, Steven H. Abman16, Eric D. Austin5 and Olivier Danhaive17,18 @ERSpublications TBX4 mutations and deletions are associated with abnormal distal lung development, persistent pulmonary hypertension of the newborn, paediatric pulmonary hypertension, multiple congenital anomalies and developmental disabilities http://bit.ly/2UXDrl3 Cite this article as: Galambos C, Mullen MP, Shieh JT, et al. Phenotype characterisation of TBX4 mutation and deletion carriers with neonatal and paediatric pulmonary hypertension. Eur Respir J 2019; 54: 1801965 [https://doi.org/10.1183/13993003.01965-2018]. ABSTRACT Rare variants in the T-box transcription factor 4 gene (TBX4) have recently been recognised as an emerging cause of paediatric pulmonary hypertension (PH). Their pathophysiology and contribution to persistent pulmonary hypertension in neonates (PPHN) are unknown. We sought to define the spectrum of clinical manifestations and histopathology associated with TBX4 variants in neonates and children with PH. We assessed clinical data and lung tissue in 19 children with PH, including PPHN, carrying TBX4 rare variants identified by next-generation sequencing and copy number variation arrays. Variants included six 17q23 deletions encompassing the entire TBX4 locus and neighbouring genes, and 12 likely damaging mutations. 10 infants presented with neonatal hypoxic respiratory failure and PPHN, and were subsequently discharged home.
[Show full text]
High-Density Array Comparative Genomic Hybridization Detects Novel Copy Number Alterations in Gastric Adenocarcinoma
ANTICANCER RESEARCH 34: 6405-6416 (2014) High-density Array Comparative Genomic Hybridization Detects Novel Copy Number Alterations in Gastric Adenocarcinoma ALINE DAMASCENO SEABRA1,2*, TAÍSSA MAÍRA THOMAZ ARAÚJO1,2*, FERNANDO AUGUSTO RODRIGUES MELLO JUNIOR1,2, DIEGO DI FELIPE ÁVILA ALCÂNTARA1,2, AMANDA PAIVA DE BARROS1,2, PAULO PIMENTEL DE ASSUMPÇÃO2, RAQUEL CARVALHO MONTENEGRO1,2, ADRIANA COSTA GUIMARÃES1,2, SAMIA DEMACHKI2, ROMMEL MARIO RODRÍGUEZ BURBANO1,2 and ANDRÉ SALIM KHAYAT1,2 1Human Cytogenetics Laboratory and 2Oncology Research Center, Federal University of Pará, Belém Pará, Brazil Abstract. Aim: To investigate frequent quantitative alterations gastric cancer is the second most frequent cancer in men and of intestinal-type gastric adenocarcinoma. Materials and the third in women (4). The state of Pará has a high Methods: We analyzed genome-wide DNA copy numbers of 22 incidence of gastric adenocarcinoma and this disease is a samples and using CytoScan® HD Array. Results: We identified public health problem, since mortality rates are above the 22 gene alterations that to the best of our knowledge have not Brazilian average (5). been described for gastric cancer, including of v-erb-b2 avian This tumor can be classified into two histological types, erythroblastic leukemia viral oncogene homolog 4 (ERBB4), intestinal and diffuse, according to Laurén (4, 6, 7). The SRY (sex determining region Y)-box 6 (SOX6), regulator of intestinal type predominates in high-risk areas, such as telomere elongation helicase 1 (RTEL1) and UDP- Brazil, and arises from precursor lesions, whereas the diffuse Gal:betaGlcNAc beta 1,4- galactosyltransferase, polypeptide 5 type has a similar distribution in high- and low-risk areas and (B4GALT5).
[Show full text]
Structural Studies on Mammalian Septins – New Insights Into Filament Formation
Structural studies on mammalian septins – New insights into filament formation Inaugural-Dissertation zur Erlangung des Doktorgrades des Fachbereiches Chemie der Universität Dortmund vorgelegt von Minhajuddin Sirajuddin aus Ranipet / Indien Dortmund 2007 ii Die vorliegende Arbeit wurde im Zeitraum October 2003 bis August 2007 in der Abteilung I (Structurelle Biologie) des Max-Planck-Instituts für Molekulare Physiologie in Dortmund unter der Anleitung von Prof. Dr. Alfred Wittinghofer angefertigt. 1. Gutachter: Prof. Dr. Alfred Wittinghofer 2. Gutachter: Prof. Dr. Herbert Waldmann iii iv Contents Contents 1 Introduction.................................................................................................... 1 1.1 Cytoskeleton ...................................................................................................1 1.1.1 Components of the cytoskeleton................................................................................ 1 1.1.2 Polymerization and dynamics of cytoskeletal systems.............................................. 4 1.2 An overview of the cell cycle .........................................................................5 1.3 Guanine nucleotide binding proteins ..............................................................7 1.3.1 Classification of GTPase superclass.......................................................................... 8 1.3.2 Characteristic features of the G domain .................................................................... 9 1.4 Septins identification ....................................................................................11
[Show full text]