BF0588-COTL1 Antibody

Total Page：16

File Type：pdf, Size：1020Kb

Affinity Biosciences website:www.affbiotech.com order:[email protected] COTL1 Antibody Cat.#: BF0588 Concn.: 1mg/ml Mol.Wt.: 16kDa Size: 50ul,100ul,200ul Source: Mouse Clonality: Monoclonal Application: ELISA 1:10000, WB 1:500-1:2000, IHC 1:200-1:1000 *The optimal dilutions should be determined by the end user. Reactivity: Human Purification: Affinity-chromatography. Specificity: COTL1 antibody detects endogenous levels of total COTL1. Immunogen: Purified recombinant fragment of human COTL1 expressed in E. Coli. Uniprot: Q14019 Description: This gene encodes one of the numerous actin-binding proteins which regulate the actin cytoskeleton. This protein binds F-actin, and also interacts with 5-lipoxygenase, which is the first committed enzyme in leukotriene biosynthesis. Although this gene has been reported to map to chromosome 17 in the Smith-Magenis syndrome region, the best alignments for this gene are to chromosome 16. The Smith-Magenis syndrome region is the site of two related pseudogenes. Storage Condition and Mouse IgG1 in phosphate buffered saline (without Mg2+ and Buffer: Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.Store at -20 °C.Stable for 12 months from date of receipt. Figure 2: Western blot analysis using COTL1 mAb against HEK293 (1) and COTL1 (AA: 1-142)-hIgGFc transfected HEK293 (2) cell lysate. 1 / 2 Affinity Biosciences website:www.affbiotech.com order:[email protected] Figure 1: Western blot analysis using COTL1 mAb against human COTL1 (AA: 1-142) recombinant protein. (Expected MW is 16 kDa) Figure 4: Immunohistochemical analysis of paraffin-embedded liver cancer tissues using COTL1 mouse mAb with DAB staining. Figure 3: Immunohistochemical analysis of paraffin-embedded breast cancer tissues using COTL1 mouse mAb with DAB staining. IMPORTANT: For western blot, incubate membrane with diluted primary Ab in 5% w/v milk , 1X TBS, 0.1% Tween®20 at 4°C with gentle shaking, overnight. For Research Use Only. Not for use in diagnostic and therapeutic procedures. Not for resale without express authorization. 2 / 2 Powered by TCPDF (www.tcpdf.org).

Copy Link

Recommended publications

Revealing the Acute Asthma Ignorome: Characterization and Validation of Uninvestigated Gene Networks
www.nature.com/scientificreports OPEN Revealing the acute asthma ignorome: characterization and validation of uninvestigated gene Received: 07 December 2015 Accepted: 01 April 2016 networks Published: 21 April 2016 Michela Riba1,*, Jose Manuel Garcia Manteiga1,*, Berislav Bošnjak2,*, Davide Cittaro1, Pavol Mikolka2,†, Connie Le2,‡, Michelle M. Epstein2,# & Elia Stupka1,# Systems biology provides opportunities to fully understand the genes and pathways in disease pathogenesis. We used literature knowledge and unbiased multiple data meta-analysis paradigms to analyze microarray datasets across different mouse strains and acute allergic asthma models. Our combined gene-driven and pathway-driven strategies generated a stringent signature list totaling 933 genes with 41% (440) asthma-annotated genes and 59% (493) ignorome genes, not previously associated with asthma. Within the list, we identified inflammation, circadian rhythm, lung-specific insult response, stem cell proliferation domains, hubs, peripheral genes, and super-connectors that link the biological domains (Il6, Il1ß, Cd4, Cd44, Stat1, Traf6, Rela, Cadm1, Nr3c1, Prkcd, Vwf, Erbb2). In conclusion, this novel bioinformatics approach will be a powerful strategy for clinical and across species data analysis that allows for the validation of experimental models and might lead to the discovery of novel mechanistic insights in asthma. Allergen exposure causes a complex interaction of cellular and molecular networks leading to allergic asthma in susceptible individuals. Experimental mouse models of allergic asthma are widely used to understand disease pathogenesis and elucidate mechanisms underlying the initiation of allergic asthma1. For example, gene profiling of lung tissue from experimental mice during the initiation of allergic asthma in experiments with different proto- cols2–7 validated well-known genes and identified new genes with roles in disease pathogenesis such as C53, Arg18, Adam89, and Pon17, and dissected pathways activated by Il1310 and Stat611.
[Show full text]
Novel Parent-Of-Origin-Specific Differentially Methylated Loci on Chromosome 16
CORE Metadata, citation and similar papers at core.ac.uk Provided by Digital Commons@Becker Washington University School of Medicine Digital Commons@Becker Open Access Publications 4-8-2019 Novel parent-of-origin-specific differentially methylated loci on chromosome 16 Katharina V Schulze Przemyslaw Szafranski Harry Lesmana Robert J Hopkin Aaron Hamvas See next page for additional authors Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Authors Katharina V Schulze, Przemyslaw Szafranski, Harry Lesmana, Robert J Hopkin, Aaron Hamvas, Jennifer A Wambach, Marwan Shinawi, Gladys Zapata, Claudia M B Carvalho, Qian Liu, Justyna A Karolak, James R Lupski, Neil A Hanchard, and Paweł Stankiewicz Schulze et al. Clinical Epigenetics (2019) 11:60 https://doi.org/10.1186/s13148-019-0655-8 RESEARCH Open Access Novel parent-of-origin-specific differentially methylated loci on chromosome 16 Katharina V. Schulze1†, Przemyslaw Szafranski1†, Harry Lesmana2, Robert J. Hopkin2, Aaron Hamvas3, Jennifer A. Wambach4, Marwan Shinawi5, Gladys Zapata6, Claudia M. B. Carvalho1, Qian Liu1, Justyna A. Karolak1, James R. Lupski1,6,7, Neil A. Hanchard1,8*† and Paweł Stankiewicz1*† Abstract Background: Congenital malformations associated with maternal uniparental disomy of chromosome 16, upd(16)mat, resemble those observed in newborns with the lethal developmental lung disease, alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV). Interestingly, ACDMPV-causative deletions, involving FOXF1 or its lung- specific upstream enhancer at 16q24.1, arise almost exclusively on the maternally inherited chromosome 16. Given the phenotypic similarities between upd(16)mat and ACDMPV, together with parental allelic bias in ACDMPV, we hypothesized that there may be unknown imprinted loci mapping to chromosome 16 that become functionally unmasked by chromosomal structural variants.
[Show full text]
Epigenetic Changes in Human Model KMT2A Leukemias Highlight Early Events During Leukemogenesis
Epigenetic changes in human model KMT2A leukemias highlight early events during leukemogenesis Thomas Milan1, Magalie Celton1, Karine Lagacé1, Élodie Roques1, Safia Safa-Tahar-Henni1, Eva Bresson2,3,4, Anne Bergeron2,3,4, Josée Hebert5,6, Soheil Meshinchi7, Sonia Cellot8, Frédéric Barabé2,3,4, 1,6 Brian T Wilhelm Author contributions: BTW and TM designed the study, analyzed data and drafted the manuscript. TM and KL performed ChIP-seq and ATAC-seq, analysed the data and generated figures. MC performed Methyl-seq experiments, analysed data, generated figures and drafted the manuscript. SS-T-H assisted with the ATAC-seq analysis and generation of figures. KL, ER, EB, and AB helped with molecular biology work, cloning and cell culture. EB, AB and FB generated the model on mice from CD34+ cells. SM provided expression and clinical data for patient samples and JH and SC collected, characterized, and banked the local patient samples used in this study. Affiliations: 1Laboratory for High Throughput Biology, Institute for Research in Immunology and Cancer, Montréal, QC, Canada 2Centre de recherche en infectiologie du CHUL, Centre de recherche du CHU de Québec – Université Laval, Québec City, QC, Canada, 3CHU de Québec – Université Laval – Hôpital Enfant-Jésus; Québec City, QC, Canada; 4Department of Medicine, Université Laval, Quebec City, QC, Canada 5Division of Hematology-Oncology and Leukemia Cell Bank of Quebec, Maisonneuve-Rosemont Hospital, Montréal, QC, Canada, 6Department of Medicine, Université de Montréal, Montréal, QC, Canada, 7Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA 8Department of pediatrics, division of Hematology, Ste-Justine Hospital, Montréal, QC, Canada Running head: Early epigenetic changes in KM3-AML *Correspondence to: Brian T Wilhelm Institute for Research in Immunology and Cancer Université de Montréal P.O.
[Show full text]
The Role O F Human Coactosin
https://doi.org/10.33805/2638-7735.107 Volume 1 Issue 1 | PDF 107 | Pages 5 Volume 1 . Issue 1 | PDF 101 | Page 1 of x Biochemistry and Modern Applications Review Article ISSN: 2638-7735 The Role of Human Coactosin-Like Protein in Neurodegenerative Disorders 1,4, 5 2,3,5 1,3,4,5* Y Anu Shanu , Antonio Lauto , Simon J Myers Affiliation 1Neuro-Cell Biology Laboratory, Western Sydney University, Locked Bag 1797, Penrith, NSW 1797 Australia 2Biomedical Engineering & Neuroscience (BENS), Western Sydney University, Locked Bag 1797, Penrith South DC, NSW 1797 Australia 3School of Science and Health, Western Sydney University, Locked Bag 1797, Penrith, NSW 1797 Australia 4Medical Sciences Research Group, School of Medicine, Western Sydney University, Locked Bag 1797, Penrith, NSW 1797 Australia 5School of Medicine, Western Sydney University, Locked Bag 1797, Penrith, NSW 1797 Australia *Corresponding author: Simon J Myers, Neuro-Cell Biology Laboratory, Western Sydney University, Locked Bag 1797, Penrith, NSW 1797 Australia, Tel: +61-2-46203383, Fax: +61-2-46203025, Email: [email protected] Citation: Anu SY, Lauto A, Myers SJ. The Role of Human Coactosin-Like Protein in Neurodegenerative Disorders (2017) Biochemistry and Modern Applications 1: 20-24. Received: Nov 27, 2017 Accepted: Dec 26, 2017 Published: Dec 31, 2017 Copyright: © 2017 Myers SJ, et al., This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Coactosin is one of the numerous actin-binding proteins which regulate the actin cytoskeleton.
[Show full text]
Analysis and Functional Evaluation of the Hair-Cell Transcriptome
Analysis and functional evaluation of the hair-cell transcriptome Brian M. McDermott, Jr.*, Jessica M. Baucom, and A. J. Hudspeth† Howard Hughes Medical Institute and Laboratory of Sensory Neuroscience, The Rockefeller University, 1230 York Avenue, New York, NY 10021-6399 Contributed by A. J. Hudspeth, May 17, 2007 (sent for review March 31, 2007) An understanding of the molecular bases of the morphogenesis, ciated from the lagena, a receptor organ of the zebrafish’s ear. organization, and functioning of hair cells requires that the genes Linear amplification of the RNA from 200 hair cells yielded Ϸ40 expressed in these cells be identified and their functions ascer- ␮g of aRNA, an enhancement of Ϸ1 millionfold. The resultant tained. After purifying zebrafish hair cells and detecting mRNAs labeled aRNA was hybridized to an Affymetrix microarray with oligonucleotide microarrays, we developed a subtractive (Affymetrix, Santa Clara, CA) containing Ϸ15,000 oligonucle- strategy that identified 1,037 hair cell-expressed genes whose otide probe sets. Averaging the outcomes of three experiments cognate proteins subserve functions including membrane trans- (SI Data Set 1) resulted in the identification of 6,472 transcripts port, synaptic transmission, transcriptional control, cellular adhe- scored as ‘‘present’’ (SI Data Set 2). sion and signal transduction, and cytoskeletal organization. To In the second step, we defined the transcriptome from cells of assess the validity of the subtracted hair-cell data set, we verified a nonsensory organ, the liver (SI Data Set 1). Hepatocytes were the presence of 11 transcripts in inner-ear tissue. Functional eval- selected for the subtraction process for three reasons: they are uation of two genes from the subtracted data set revealed their nonneuronal and thus unlikely to express synaptic factors; they importance in hair bundles: zebrafish larvae bearing the seahorse lack cilia (http://members.global2000.net/bowser/cilialist.html) and ift 172 mutations display specific kinociliary defects.
[Show full text]
Discriminating Mild from Critical COVID-19 by Innate and Adaptive Immune Single-Cell Profiling of Bronchoalveolar Lavages
www.nature.com/cr www.cell-research.com ARTICLE OPEN Discriminating mild from critical COVID-19 by innate and adaptive immune single-cell profiling of bronchoalveolar lavages Els Wauters1,2, Pierre Van Mol 2,3,4, Abhishek Dinkarnath Garg 5, Sander Jansen 6, Yannick Van Herck7, Lore Vanderbeke8, Ayse Bassez3,4, Bram Boeckx3,4, Bert Malengier-Devlies 9, Anna Timmerman3,4, Thomas Van Brussel3,4, Tina Van Buyten6, Rogier Schepers3,4, Elisabeth Heylen 6, Dieter Dauwe 10, Christophe Dooms1,2, Jan Gunst10, Greet Hermans10, Philippe Meersseman11, Dries Testelmans1,2, Jonas Yserbyt1,2, Sabine Tejpar12, Walter De Wever13, Patrick Matthys 9, CONTAGIOUS collaborators, Johan Neyts6, Joost Wauters11, Junbin Qian14 and Diether Lambrechts 3,4 How the innate and adaptive host immune system miscommunicate to worsen COVID-19 immunopathology has not been fully elucidated. Here, we perform single-cell deep-immune profiling of bronchoalveolar lavage (BAL) samples from 5 patients with mild and 26 with critical COVID-19 in comparison to BALs from non-COVID-19 pneumonia and normal lung. We use pseudotime inference to build T-cell and monocyte-to-macrophage trajectories and model gene expression changes along them. In mild + + COVID-19, CD8 resident-memory (TRM) and CD4 T-helper-17 (TH17) cells undergo active (presumably antigen-driven) expansion towards the end of the trajectory, and are characterized by good effector functions, while in critical COVID-19 they remain more + + naïve. Vice versa, CD4 T-cells with T-helper-1 characteristics (TH1-like) and CD8 T-cells expressing exhaustion markers (TEX-like) are 1234567890();,: enriched halfway their trajectories in mild COVID-19, where they also exhibit good effector functions, while in critical COVID-19 they show evidence of inflammation-associated stress at the end of their trajectories.
[Show full text]
Vast Human-Specific Delay in Cortical Ontogenesis Associated With
Supplementary information Extension of cortical synaptic development distinguishes humans from chimpanzees and macaques Supplementary Methods Sample collection We used prefrontal cortex (PFC) and cerebellar cortex (CBC) samples from postmortem brains of 33 human (aged 0-98 years), 14 chimpanzee (aged 0-44 years) and 44 rhesus macaque individuals (aged 0-28 years) (Table S1). Human samples were obtained from the NICHD Brain and Tissue Bank for Developmental Disorders at the University of Maryland, USA, the Netherlands Brain Bank, Amsterdam, Netherlands and the Chinese Brain Bank Center, Wuhan, China. Informed consent for use of human tissues for research was obtained in writing from all donors or their next of kin. All subjects were defined as normal by forensic pathologists at the corresponding brain bank. All subjects suffered sudden death with no prolonged agonal state. Chimpanzee samples were obtained from the Yerkes Primate Center, GA, USA, the Anthropological Institute & Museum of the University of Zürich-Irchel, Switzerland and the Biomedical Primate Research Centre, Netherlands (eight Western chimpanzees, one Central/Eastern and five of unknown origin). Rhesus macaque samples were obtained from the Suzhou Experimental Animal Center, China. All non-human primates used in this study suffered sudden deaths for reasons other than their participation in this study and without any relation to the tissue used. CBC dissections were made from the cerebellar cortex. PFC dissections were made from the frontal part of the superior frontal gyrus. All samples contained an approximately 2:1 grey matter to white matter volume ratio. RNA microarray hybridization RNA isolation, hybridization to microarrays, and data preprocessing were performed as described previously (Khaitovich et al.
[Show full text]
Poised Cell Circuits in Human Skin Are Activated in Disease Gary Reynolds1†, Peter Vegh1†, James Fletcher1†, Elizabeth F.M
bioRxiv preprint doi: https://doi.org/10.1101/2020.11.05.369363; this version posted November 5, 2020. 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. Poised cell circuits in human skin are activated in disease Gary Reynolds1†, Peter Vegh1†, James Fletcher1†, Elizabeth F.M. Poyner1,2†, Emily Stephenson1, Issac Goh1, Rachel A. Botting1, Ni Huang3, Bayanne Olabi1,4, Anna Dubois1,2, David Dixon1, Kile Green1, Daniel Maunder1, Justin Engelbert1, Mirjana Efremova3, Krzysztof Polański3, Laura Jardine1, Claire Jones1, Thomas Ness1, Dave Horsfall1, Jim McGrath1, Christopher Carey1, Dorin-Mirel Popescu1, Simone Webb1, Xiao-nong Wang1, Ben Sayer1, Jong-Eun Park3, Victor A. Negri5, Daria Belokhvostova5, Magnus Lynch5, David McDonald1, Andrew Filby1, Tzachi Hagai3, Kerstin B. Meyer3, Akhtar Husain6, Jonathan Coxhead1, Roser Vento-Tormo3, Sam Behjati3,7, Steven Lisgo1, Alexandra-Chloé Villani8, Jaume Bacardit9, Phil Jones3,10, Edel A. O’Toole11, Graham S. Ogg12, Neil Rajan1,2, Nick J. Reynolds2,13, Sarah A. Teichmann3,14*, Fiona Watt5*, Muzlifah Haniffa1,2,3* Affiliations: 1Biosciences Institute, Newcastle University, Newcastle upon Tyne, NE2 4HH, UK 2Department of Dermatology and NIHR Newcastle Biomedical Research Centre, Newcastle Hospitals NHS Foundation Trust, Newcastle upon Tyne NE2 4LP, UK 3Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge CB10 1SA, UK 4Department of Dermatology, NHS Lothian, Lauriston Building,
[Show full text]
Table S1. 103 Ferroptosis-Related Genes Retrieved from the Genecards
Table S1. 103 ferroptosis-related genes retrieved from the GeneCards. Gene Symbol Description Category GPX4 Glutathione Peroxidase 4 Protein Coding AIFM2 Apoptosis Inducing Factor Mitochondria Associated 2 Protein Coding TP53 Tumor Protein P53 Protein Coding ACSL4 Acyl-CoA Synthetase Long Chain Family Member 4 Protein Coding SLC7A11 Solute Carrier Family 7 Member 11 Protein Coding VDAC2 Voltage Dependent Anion Channel 2 Protein Coding VDAC3 Voltage Dependent Anion Channel 3 Protein Coding ATG5 Autophagy Related 5 Protein Coding ATG7 Autophagy Related 7 Protein Coding NCOA4 Nuclear Receptor Coactivator 4 Protein Coding HMOX1 Heme Oxygenase 1 Protein Coding SLC3A2 Solute Carrier Family 3 Member 2 Protein Coding ALOX15 Arachidonate 15-Lipoxygenase Protein Coding BECN1 Beclin 1 Protein Coding PRKAA1 Protein Kinase AMP-Activated Catalytic Subunit Alpha 1 Protein Coding SAT1 Spermidine/Spermine N1-Acetyltransferase 1 Protein Coding NF2 Neurofibromin 2 Protein Coding YAP1 Yes1 Associated Transcriptional Regulator Protein Coding FTH1 Ferritin Heavy Chain 1 Protein Coding TF Transferrin Protein Coding TFRC Transferrin Receptor Protein Coding FTL Ferritin Light Chain Protein Coding CYBB Cytochrome B-245 Beta Chain Protein Coding GSS Glutathione Synthetase Protein Coding CP Ceruloplasmin Protein Coding PRNP Prion Protein Protein Coding SLC11A2 Solute Carrier Family 11 Member 2 Protein Coding SLC40A1 Solute Carrier Family 40 Member 1 Protein Coding STEAP3 STEAP3 Metalloreductase Protein Coding ACSL1 Acyl-CoA Synthetase Long Chain Family Member 1 Protein
[Show full text]
Coactosin-Like Protein Functions As a Stabilizing Chaperone for 5
Coactosin-like protein functions as a stabilizing chaperone for 5-lipoxygenase: role of tryptophan 102 Julia Esser, Marija Rakonjac, Bettina Hofmann, Lutz Fischer, Patrick Provost, Gisbert Schneider, Dieter Steinhilber, Bengt Samuelsson, Olof P. Rådmark To cite this version: Julia Esser, Marija Rakonjac, Bettina Hofmann, Lutz Fischer, Patrick Provost, et al.. Coactosin-like protein functions as a stabilizing chaperone for 5-lipoxygenase: role of tryptophan 102. Biochemical Journal, Portland Press, 2009, 425 (1), pp.265-274. 10.1042/BJ20090856. hal-00479206 HAL Id: hal-00479206 https://hal.archives-ouvertes.fr/hal-00479206 Submitted on 30 Apr 2010 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. Biochemical Journal Immediate Publication. Published on 06 Oct 2009 as manuscript BJ20090856 Coactosin-like protein functions as a stabilizing chaperone for 5-lipoxygenase: role of tryptophan 102 Julia Esser1*, Marija Rakonjac1*, Bettina Hofmann3,4, Lutz Fischer1,3, Patrick Provost2, Gisbert Schneider4, Dieter Steinhilber3, Bengt Samuelsson1, and Olof Rådmark1 1. Department of Medical Biochemistry and Biophysics, Division of Physiological Chemistry II, Karolinska Institutet, S-171 77 Stockholm, Sweden 2. Centre de Recherche en Rhumatologie et Immunologie, CHUL Research Center/CHUQ, Quebec, QC, G1V 4G2, Canada 3.
[Show full text]
Novel Parent-Of-Origin-Specific Differentially Methylated Loci on Chromosome 16 Katharina V
Schulze et al. Clinical Epigenetics (2019) 11:60 https://doi.org/10.1186/s13148-019-0655-8 RESEARCH Open Access Novel parent-of-origin-specific differentially methylated loci on chromosome 16 Katharina V. Schulze1†, Przemyslaw Szafranski1†, Harry Lesmana2, Robert J. Hopkin2, Aaron Hamvas3, Jennifer A. Wambach4, Marwan Shinawi5, Gladys Zapata6, Claudia M. B. Carvalho1, Qian Liu1, Justyna A. Karolak1, James R. Lupski1,6,7, Neil A. Hanchard1,8*† and Paweł Stankiewicz1*† Abstract Background: Congenital malformations associated with maternal uniparental disomy of chromosome 16, upd(16)mat, resemble those observed in newborns with the lethal developmental lung disease, alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV). Interestingly, ACDMPV-causative deletions, involving FOXF1 or its lung- specific upstream enhancer at 16q24.1, arise almost exclusively on the maternally inherited chromosome 16. Given the phenotypic similarities between upd(16)mat and ACDMPV, together with parental allelic bias in ACDMPV, we hypothesized that there may be unknown imprinted loci mapping to chromosome 16 that become functionally unmasked by chromosomal structural variants. Results: To identify parent-of-origin biased DNA methylation, we performed high-resolution bisulfite sequencing of chromosome 16 on peripheral blood and cultured skin fibroblasts from individuals with maternal or paternal upd(16) as well as lung tissue from patients with ACDMPV-causative 16q24.1 deletions and a normal control. We identified 22 differentially methylated regions (DMRs) with ≥ 5 consecutive CpG methylation sites and varying tissue-specificity, including the known DMRs associated with the established imprinted gene ZNF597 and DMRs supporting maternal methylation of PRR25, thought to be paternally expressed in lymphoblastoid cells.
[Show full text]
Studies on the Regulation of Leukotriene Biosynthesis in Antigen Presenting Cells
Department of Medical Biochemistry and Biophysics Karolinska Institutet Stockholm, Sweden Studies on the Regulation of Leukotriene Biosynthesis in Antigen Presenting Cells Julia Esser Stockholm, 2011 Fur¨ Arndt All previously published papers were reproduced with the permission from the publishers. PhD thesis, Published by Karolinska Institutet, Printed by Larserics c Julia Esser, 2011 ISBN 978-91-7457-272-8 Die Verletzten sollen die Arzte¨ sein Die Letzten sollen die Ersten sein Die Ersten sehen als Letzte ein: The geek shall inherit the earth (Wir sind Helden) Summary Leukotrienes (LTs) are pro-inflammatory lipid mediators with important roles in host de- fense and inflammatory disease. Leukotriene B4 (LTB4) is a potent chemoattractant for neutrophils and contributes to bacterial killing, while the cysteinyl leukotrienes (LTC4, LTD4 and LTE4) elicit increased vascular permeability, bronchoconstriction, eosinophil trafficking and mucus secretion. Due to their potency to trigger inflammatory responses, the biosynthesis of LTs is highly regulated. This regulation aids to proper pathogen clear- ance and simultaneously prevents the development of chronic inflammation. It was the aim of this thesis to contribute to a better understanding of the regulatory mechanisms that control LT biosynthesis. 5-lipoxygenase (5-LO), the first enzyme of the LT biosynthetic pathway, catalyzes the conversion of arachidonic acid (AA) to the intermediate leukotriene A4 (LTA4). Here, we describe a function of coactosin like protein (CLP) as a stabilizing chaperone for 5-LO. We found that the interaction of 5-LO with CLP, which protects the enzyme from inactivation, depends on lysine 131 in CLP and tryptophan 102 in the regulatory domain of 5-LO.
[Show full text]