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Calreticulin Controlling the Membrane Translocation of Immunogenicity Of
ERP57 Membrane Translocation Dictates the Immunogenicity of Tumor Cell Death by Controlling the Membrane Translocation of Calreticulin This information is current as of September 25, 2021. Michel Obeid J Immunol 2008; 181:2533-2543; ; doi: 10.4049/jimmunol.181.4.2533 http://www.jimmunol.org/content/181/4/2533 Downloaded from References This article cites 26 articles, 11 of which you can access for free at: http://www.jimmunol.org/content/181/4/2533.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 25, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2008 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology ERP57 Membrane Translocation Dictates the Immunogenicity of Tumor Cell Death by Controlling the Membrane Translocation of Calreticulin1 Michel Obeid2 Several pieces of experimental evidence indicate the following: 1) the most efficient antitumor treatments (this principle applies on both chemotherapy and radiotherapy) are those that induce immunogenic cell death and are able to trigger a specific antitumor immune response; and 2) the immunogenicity of cell death depends very closely on the plasma membrane quantity of calreticulin (CRT), an endoplasmic reticulum (ER) stress protein exposed to the cell membrane after immunogenic treatment. -
Pnas11138correction 14002..14003
Corrections MEDICAL SCIENCES Correction for “Regulation of bone remodeling by vasopressin New, Alberta Zallone, and Mone Zaidi, which appeared in issue 46, explains the bone loss in hyponatremia,” by Roberto Tamma, November 12, 2013, of Proc Natl Acad Sci USA (110:18644–18649; Li Sun, Concetta Cuscito, Ping Lu, Michelangelo Corcelli, first published October 28, 2013; 10.1073/pnas.1318257110). Jianhua Li, Graziana Colaianni, Surinder S. Moonga, Adriana The authors note that Fig. 1 appeared incorrectly. The cor- Di Benedetto, Maria Grano, Silvia Colucci, Tony Yuen, Maria I. rected figure and its legend appear below. Fig. 1. Bone cells express Avprs. Immunofluorescence micrographs (A) and Western immunoblotting (B) show the expression of Avpr1α in osteoblasts and osteoclasts, and as a function of osteoblast (mineralization) and osteoclast (with Rankl) differentiation. The expression of Avp (ligand) and Avpr1α (receptor) in osteoblasts is regulated by 17β-estradiol, as determined by quantitative PCR (C) and Western immunoblotting (D). (Magnification: A,63×.) Because Avp is a small peptide, its precursor neurophysin II is measured. Statistics: Student t test, P values shown compared with 0 h. Stimulation of Erk phosphorylation − (p-Erk) as a function of total Erk (t-Erk) by Avp (10 8 M) in osteoclast precursors (preosteoclasts), osteoclasts (OC), and osteoblasts establishes functionality of − the Avpr1α in the presence or absence of the receptor inhibitor SR49059 (10 8 M) (E). Western immunoblotting showing the expression of Avpr2 in pre- −/− osteoclasts, OCs (F), and osteoblasts (G) isolated from Avpr1α mice, as well as in MC3T3.E1 osteoblast precursors (G). Functionality of Avpr2 was confirmed −/− by the demonstration that cells from Avpr1α mice remained responsive to AVP in reducing the expression of osteoblast differentiation genes, namely Runx2, Osx, Bsp, Atf4, Opn, and Osteocalcin (quantitative PCR, P values shown) (H). -
Sat-196 How to Estimate Glomerular Filtration Rate
ISN WCN 2019 ABSTRACTS 13 (28%) patients had CKD stage 3. 6/13 had low predicted risk of Nephrology, Melbourne, Australia, 8Austin Hospital, Nephrology, Heidel- berg, Australia, 9Monash Childrens Hospital, Nephrology, Australia, progression at 5 years of whom 4/6 progressed unexpectedly. 1/13 was 10 identified as having high risk at 5 years and that 1 patient progressed to Melbourne Genomics Health Alliance, Victorian Clinical Genetics Service, Melbourne, Australia, 11Australian Genomic Health Alliance, KidGen Renal CKD5D/T. Genetics Flagship, Australia, Australia, 12Royal Childrens Hospital, 6/18 CKD 3/4 patients with predicted low risk progressed to CKD5D/ Nephrology, Melbourne, Australia T unexpectedly. 1/6 had emergency abdominal surgery, 1/6 patient had Introduction: Genomic technologies enable the rapid and cost-effective unexplained rapid progression and 4/6 had acute upper gastro-intes- fi tinal haemorrhage causing terminal decline of kidney function. sequencing of DNA and have demonstrated a de nitive diagnosis in Conclusions: The number of patients analysed was small. The 8-vari- several patient groups. The clinical utility of whole exome sequencing able equation accurately predicted high risk of progression to CKD5D/T (WES) in a kidney disease cohort is not yet well established. We in 7/9 CKD3/4 patients. describe the patient characteristics and diagnostic yield of a cohort of Conversely, 6/18 patients with predicted low risk progressed to 200 patients with suspected genetic kidney disease referred for WES via CKD5D/T. Acute medical events including upper gastro-intestinal bleed a multidisciplinary renal genetics clinic. Methods: accounted for most instances of unexpected progression. 200 sequential patients were recruited into a prospective observational cohort study through five tertiary academic centres in Victoria, Australia. -
The Atf6β-Calreticulin Axis Promotes Neuronal Survival Under Endoplasmic Reticulum Stress and Excitotoxicity
bioRxiv preprint doi: https://doi.org/10.1101/2021.02.01.429116; this version posted February 2, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 1 1 The ATF6β-calreticulin axis promotes neuronal survival under 2 endoplasmic reticulum stress and excitotoxicity 3 4 Dinh Thi Nguyen1, Thuong Manh Le1, Tsuyoshi Hattori1, Mika Takarada-Iemata1, 5 Hiroshi Ishii1, Jureepon Roboon1, Takashi Tamatani1, Takayuki Kannon2, 6 Kazuyoshi Hosomichi2, Atsushi Tajima2, Shusuke Taniuchi3, Masato Miyake3, Seiichi 7 Oyadomari3, Shunsuke Saito4, Kazutoshi Mori4, Osamu Hori1* 8 9 10 1.Department of Neuroanatomy, Graduate School of Medical Sciences, Kanazawa 11 University, Kanazawa, Japan 12 2.Department of Bioinformatics and Genomics, Graduate School of Advanced Preventive 13 Medical Sciences, Kanazawa University, Kanazawa, Japan 14 3.Division of Molecular Biology, Institute for Genome Research, Institute of Advanced 15 Medical Sciences, Tokushima University, Tokushima, Japan 16 4.Department of Biophysics, Graduate School of Science, Kyoto University, Kyoto, Japan 17 18 19 Running title: Neuroprotective role of the ATF6β-calreticulin axis 20 21 22 23 24 25 26 * Corresponding author: 27 Dr. Osamu Hori 28 Department of Neuroanatomy, Kanazawa University Graduate School of Medical 29 Sciences, 30 13-1 Takara-Machi, Kanazawa City, 31 Ishikawa 920-8640, Japan 32 Tel: +81-76-265-2162 33 Fax: +81-76-234-4222 34 E-mail: [email protected] 35 36 37 38 39 Key words: neurodegeneration, Ca2+ homeostasis, ER stress 40 bioRxiv preprint doi: https://doi.org/10.1101/2021.02.01.429116; this version posted February 2, 2021. -
Calreticulin—Multifunctional Chaperone in Immunogenic Cell Death: Potential Significance As a Prognostic Biomarker in Ovarian
cells Review Calreticulin—Multifunctional Chaperone in Immunogenic Cell Death: Potential Significance as a Prognostic Biomarker in Ovarian Cancer Patients Michal Kielbik *, Izabela Szulc-Kielbik and Magdalena Klink Institute of Medical Biology, Polish Academy of Sciences, 106 Lodowa Str., 93-232 Lodz, Poland; [email protected] (I.S.-K.); [email protected] (M.K.) * Correspondence: [email protected]; Tel.: +48-42-27-23-636 Abstract: Immunogenic cell death (ICD) is a type of death, which has the hallmarks of necroptosis and apoptosis, and is best characterized in malignant diseases. Chemotherapeutics, radiotherapy and photodynamic therapy induce intracellular stress response pathways in tumor cells, leading to a secretion of various factors belonging to a family of damage-associated molecular patterns molecules, capable of inducing the adaptive immune response. One of them is calreticulin (CRT), an endoplasmic reticulum-associated chaperone. Its presence on the surface of dying tumor cells serves as an “eat me” signal for antigen presenting cells (APC). Engulfment of tumor cells by APCs results in the presentation of tumor’s antigens to cytotoxic T-cells and production of cytokines/chemokines, which activate immune cells responsible for tumor cells killing. Thus, the development of ICD and the expression of CRT can help standard therapy to eradicate tumor cells. Here, we review the physiological functions of CRT and its involvement in the ICD appearance in malignant dis- ease. Moreover, we also focus on the ability of various anti-cancer drugs to induce expression of surface CRT on ovarian cancer cells. The second aim of this work is to discuss and summarize the prognostic/predictive value of CRT in ovarian cancer patients. -
Steroid-Dependent Regulation of the Oviduct: a Cross-Species Transcriptomal Analysis
University of Kentucky UKnowledge Theses and Dissertations--Animal and Food Sciences Animal and Food Sciences 2015 Steroid-dependent regulation of the oviduct: A cross-species transcriptomal analysis Katheryn L. Cerny University of Kentucky, [email protected] Right click to open a feedback form in a new tab to let us know how this document benefits ou.y Recommended Citation Cerny, Katheryn L., "Steroid-dependent regulation of the oviduct: A cross-species transcriptomal analysis" (2015). Theses and Dissertations--Animal and Food Sciences. 49. https://uknowledge.uky.edu/animalsci_etds/49 This Doctoral Dissertation is brought to you for free and open access by the Animal and Food Sciences at UKnowledge. It has been accepted for inclusion in Theses and Dissertations--Animal and Food Sciences by an authorized administrator of UKnowledge. For more information, please contact [email protected]. STUDENT AGREEMENT: I represent that my thesis or dissertation and abstract are my original work. Proper attribution has been given to all outside sources. I understand that I am solely responsible for obtaining any needed copyright permissions. I have obtained needed written permission statement(s) from the owner(s) of each third-party copyrighted matter to be included in my work, allowing electronic distribution (if such use is not permitted by the fair use doctrine) which will be submitted to UKnowledge as Additional File. I hereby grant to The University of Kentucky and its agents the irrevocable, non-exclusive, and royalty-free license to archive and make accessible my work in whole or in part in all forms of media, now or hereafter known. -
Comparative Analysis of a Teleost Skeleton Transcriptome Provides Insight Into Its Regulation
Accepted Manuscript Comparative analysis of a teleost skeleton transcriptome provides insight into its regulation Florbela A. Vieira, M.A.S. Thorne, K. Stueber, M. Darias, R. Reinhardt, M.S. Clark, E. Gisbert, D.M. Power PII: S0016-6480(13)00264-5 DOI: http://dx.doi.org/10.1016/j.ygcen.2013.05.025 Reference: YGCEN 11541 To appear in: General and Comparative Endocrinology Please cite this article as: Vieira, F.A., Thorne, M.A.S., Stueber, K., Darias, M., Reinhardt, R., Clark, M.S., Gisbert, E., Power, D.M., Comparative analysis of a teleost skeleton transcriptome provides insight into its regulation, General and Comparative Endocrinology (2013), doi: http://dx.doi.org/10.1016/j.ygcen.2013.05.025 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. 1 Comparative analysis of a teleost skeleton transcriptome 2 provides insight into its regulation 3 4 Florbela A. Vieira1§, M. A. S. Thorne2, K. Stueber3, M. Darias4,5, R. Reinhardt3, M. 5 S. Clark2, E. Gisbert4 and D. M. Power1 6 7 1Center of Marine Sciences, Universidade do Algarve, Faro, Portugal. 8 2British Antarctic Survey – Natural Environment Research Council, High Cross, 9 Madingley Road, Cambridge, CB3 0ET, UK. -
Gene Alterations Identified by Expression Profiling in Tumor-Associated Endothelial Cells from Invasive Ovarian Carcinoma
Research Article Gene Alterations Identified by Expression Profiling in Tumor-Associated Endothelial Cells from Invasive Ovarian Carcinoma Chunhua Lu,1 Tomas Bonome,3 Yang Li,1 Aparna A. Kamat,1 Liz Y. Han,1 Rosemarie Schmandt,1 Robert L. Coleman,1 David M. Gershenson,1 Robert B. Jaffe,4 MichaelJ. Birrer, 3 and AnilK. Sood 1,2 Departments of 1Gynecologic Oncology and 2Cancer Biology, University of Texas M. D. Anderson Cancer Center, Houston, Texas; 3Cell and Cancer Biology Branch, National Cancer Institute, Bethesda, Maryland; and 4Center for Reproductive Sciences, University of California, San Francisco, San Francisco, California Abstract the promise of such approaches. However, the full spectrum of Therapeutic strategies based on antiangiogenic approaches differences in the tumor vasculature compared with its normal are beginning to show great promise in clinical studies. counterpart is not known. Identification of additional targets on However, full realization of these approaches requires tumor endothelium may allow opportunities for developing new identification of key differences in gene expression between therapeutic approaches to inhibit angiogenesis in a tumor-specific endothelial cells from tumors versus their normal counter- manner. parts. Here, we examined gene expression differences in Higher levels of proangiogenic cytokines and angiogenesis are purified endothelial cells from 10invasive epithelial ovarian associated with an increased risk of metastasis and poor prognosis cancers and 5 normal ovaries using Affymetrix U133 Plus in ovarian cancer (5, 6). To date, a small number of breast, colon, 2.0microarrays. More than 400differentially expressed genes and brain cancers have been analyzed for gene expression changes were identified in tumor-associated endothelial cells. -
Annexin A1 Released in Extracellular Vesicles by Pancreatic Cancer Cells Activates Components of the Tumor Microenvironment
cells Article Annexin A1 Released in Extracellular Vesicles by Pancreatic Cancer Cells Activates Components of the Tumor Microenvironment, through Interaction with the Formyl-Peptide Receptors Nunzia Novizio 1, Raffaella Belvedere 1 , Emanuela Pessolano 1,2 , Alessandra Tosco 1 , Amalia Porta 1 , Mauro Perretti 2, Pietro Campiglia 1 , Amelia Filippelli 3 and Antonello Petrella 1,* 1 Department of Pharmacy, University of Salerno, Via Giovanni Paolo II 132, 84084 Fisciano, Italy; [email protected] (N.N.); [email protected] (R.B.); [email protected] (E.P.); [email protected] (A.T.); [email protected] (A.P.); [email protected] (P.C.) 2 The William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK; [email protected] 3 Department of Medicine, Surgery and Dentistry, University of Salerno, Via S. Allende 43, 84081 Baronissi, Italy; afi[email protected] * Correspondence: [email protected]; Tel.: +39-089-969-762; Fax: +39-089-969-602 Received: 17 November 2020; Accepted: 17 December 2020; Published: 18 December 2020 Abstract: Pancreatic cancer (PC) is one of the most aggressive cancers in the world. Several extracellular factors are involved in its development and metastasis to distant organs. In PC, the protein Annexin A1 (ANXA1) appears to be overexpressed and may be identified as an oncogenic factor, also because it is a component in tumor-deriving extracellular vesicles (EVs). Indeed, these microvesicles are known to nourish the tumor microenvironment. Once we evaluated the autocrine role of ANXA1-containing EVs on PC MIA PaCa-2 cells and their pro-angiogenic action, we investigated the ANXA1 paracrine effect on stromal cells like fibroblasts and endothelial ones. -
Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase -
Transcriptomic Landscape of Breast Cancers Through Mrna Sequencing Jeyanthy Eswaran George Washington University
Himmelfarb Health Sciences Library, The George Washington University Health Sciences Research Commons Biochemistry and Molecular Medicine Faculty Biochemistry and Molecular Medicine Publications 2-14-2012 Transcriptomic landscape of breast cancers through mRNA sequencing Jeyanthy Eswaran George Washington University Dinesh Cyanam George Washington University Prakriti Mudvari George Washington University Sirigiri Divijendra Natha Reddy George Washington University Suresh Pakala George Washington University See next page for additional authors Follow this and additional works at: http://hsrc.himmelfarb.gwu.edu/smhs_biochem_facpubs Part of the Biochemistry, Biophysics, and Structural Biology Commons Recommended Citation Eswaran, J., Cyanam, D., Mudvari, P., Reddy, S., Pakala, S., Nair, S., Florea, L., & Fuqua, S. (2012). Transcriptomic landscape of breast cancers through mrna sequencing. Scientific Reports, 2, 264. This Journal Article is brought to you for free and open access by the Biochemistry and Molecular Medicine at Health Sciences Research Commons. It has been accepted for inclusion in Biochemistry and Molecular Medicine Faculty Publications by an authorized administrator of Health Sciences Research Commons. For more information, please contact [email protected]. Authors Jeyanthy Eswaran, Dinesh Cyanam, Prakriti Mudvari, Sirigiri Divijendra Natha Reddy, Suresh Pakala, Sujit S. Nair, Liliana Florea, Suzanne A.W. Fuqua, Sucheta Godbole, and Rakesh Kumar This journal article is available at Health Sciences Research Commons: http://hsrc.himmelfarb.gwu.edu/smhs_biochem_facpubs/3 -
Changes in the Cytosolic Proteome of Aedes Malpighian Tubules
329 The Journal of Experimental Biology 212, 329-340 Published by The Company of Biologists 2009 doi:10.1242/jeb.024646 Research article Signaling to the apical membrane and to the paracellular pathway: changes in the cytosolic proteome of Aedes Malpighian tubules Klaus W. Beyenbach1,*, Sabine Baumgart2, Kenneth Lau1, Peter M. Piermarini1 and Sheng Zhang2 1Department of Biomedical Sciences, VRT 8004, Cornell University, Ithaca, NY 14853, USA and 2Proteomics and Mass Spectrometry Core Facility, 143 Biotechnology Building, Cornell University, Ithaca, NY 14853, USA *Author for correspondence (e-mail: [email protected]) Accepted 6 November 2008 Summary Using a proteomics approach, we examined the post-translational changes in cytosolic proteins when isolated Malpighian tubules of Aedes aegypti were stimulated for 1 min with the diuretic peptide aedeskinin-III (AK-III, 10–7 mol l–1). The cytosols of control (C) and aedeskinin-treated (T) tubules were extracted from several thousand Malpighian tubules, subjected to 2-D electrophoresis and stained for total proteins and phosphoproteins. The comparison of C and T gels was performed by gel image analysis for the change of normalized spot volumes. Spots with volumes equal to or exceeding C/T ratios of ±1.5 were robotically picked for in- gel digestion with trypsin and submitted for protein identification by nanoLC/MS/MS analysis. Identified proteins covered a wide range of biological activity. As kinin peptides are known to rapidly stimulate transepithelial secretion of electrolytes and water by Malpighian tubules, we focused on those proteins that might mediate the increase in transepithelial secretion. We found that AK- III reduces the cytosolic presence of subunits A and B of the V-type H+ ATPase, endoplasmin, calreticulin, annexin, type II regulatory subunit of protein kinase A (PKA) and rab GDP dissociation inhibitor and increases the cytosolic presence of adducin, actin, Ca2+-binding protein regucalcin/SMP30 and actin-depolymerizing factor.