IL-33 and S100 Proteins: Dual-Function Alarmins
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Unnatural Verticilide Enantiomer Inhibits Type 2 Ryanodine Receptor-Mediated Calcium Leak and Is Antiarrhythmic
Unnatural verticilide enantiomer inhibits type 2 ryanodine receptor-mediated calcium leak and is antiarrhythmic Suzanne M. Batistea,1, Daniel J. Blackwellb,1, Kyungsoo Kimb,1, Dmytro O. Kryshtalb, Nieves Gomez-Hurtadob, Robyn T. Rebbeckc, Razvan L. Corneac, Jeffrey N. Johnstona,2, and Bjorn C. Knollmannb,2 aDepartment of Chemistry, Vanderbilt University, Nashville, TN 37235; bDepartment of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232; and cDepartment of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, MN 55455 Edited by Dale L. Boger, The Scripps Research Institute, La Jolla, CA, and approved January 15, 2019 (received for review September 27, 2018) Ca2+ leak via ryanodine receptor type 2 (RyR2) can cause poten- heart diseases associated with both atrial and ventricular arrhyth- tially fatal arrhythmias in a variety of heart diseases and has also mia (9). Mutations in RyR2 and its binding partners, which increase + been implicated in neurodegenerative and seizure disorders, mak- SR Ca2 leak, cause primary atrial and ventricular arrhythmia ing RyR2 an attractive therapeutic target for drug development. syndromes such as catecholaminergic polymorphic ventricular Here we synthesized and investigated the fungal natural product tachycardia (CPVT), providing strong evidence for the mechanistic and known insect RyR antagonist (−)-verticilide and several conge- contribution of RyR2 to arrhythmia risk in humans (10). Further ners to determine their activity against mammalian RyR2. Although support comes from gene-targeted mouse models of CPVT, where + the cyclooligomeric depsipeptide natural product (−)-verticilide had catecholamine-induced spontaneous Ca2 release from the SR no effect, its nonnatural enantiomer [ent-(+)-verticilide] signifi- via RyR2 generates potentially fatal cardiac arrhythmias (11, 12). -
Redalyc.Dysfunctional Families: One Central Theme in Two Fictional
Revista Folios ISSN: 0123-4870 [email protected] Universidad Pedagógica Nacional Colombia Gómez R., Luís Fernando Dysfunctional Families: One Central Theme in Two Fictional Works of Tony Morrison, Song of Solomon and Sula Revista Folios, núm. 29, enero-junio, 2009, pp. 119-128 Universidad Pedagógica Nacional Bogotá, Colombia Available in: http://www.redalyc.org/articulo.oa?id=345941359010 How to cite Complete issue Scientific Information System More information about this article Network of Scientific Journals from Latin America, the Caribbean, Spain and Portugal Journal's homepage in redalyc.org Non-profit academic project, developed under the open access initiative Dysfunctional Families: One Central Theme in Two Fictional Works of Tony Morrison, Song of Solomon and Sula Familias Disfuncionales: Un Tema Central en Dos Novelas de Toni Morrison, Canción de Salomón y Sula Luís Fernando Gómez R. Abstract Toni Morrison, Nobel Prize winner (1993), has been recognized as one of the most prominent novelists in the USA today. Her novels Song of Solomon and Sula rank enormous and original literary creativity through which she shows what it means to survive as an individual in the black families of America. Hence, this article explores the desperation and vulnerabilities of children who grow up in dysfunctional families and how they experience trauma and pain from their parents’ unconventional actions and behaviors. The article accounts of the irregular experiences that the main characters of these two novels have to confront at hostile homes as they grow up changed, different from other children, and lack the essential educational guidance that prepare them for adulthood. -
Association of Serum S100B, S100A1 and Zinc-Α2
Progress in Nutrition 2019; Vol. 21, Supplement 1: 154-162 DOI: 10.23751/pn.v21i1-S.5846 © Mattioli 1885 Original articles Association of serum S100B, S100A1 and Zinc-α2- Glycoprotein levels with anthropometric, metabolic and clinical indices in men and women Sorayya Kheirouri1, Mohammad Alizadeh1, Elham Ebrahimi2, Masoumeh Jabbari2 1Associate Professor, Department of Nutrition, Tabriz University of Medical Sciences, Tabriz, Iran - Email: kheirouris@tbzmed. ac.ir, [email protected]; 2MSc. student, Department of Nutrition, Tabriz University of Medical Sciences, Tabriz, Iran Summary. Objectives: We aimed to investigate serum levels of S100B, S100A1, and Zinc-α2- glycoprotein (ZAG) in men and women and to find association of these proteins with anthropometric, metabolic and clini- cal indices. Methods: Eighty-eight apparently healthy adults, 43 men and 45 women, participated in the study. The participants’ body mass index (BMI), waist circumference (WC), systolic and diastolic blood pressure (SBP and DBP) were measured. Serum levels of total cholesterol (TC), triglyceride (TG), low and high den- sity lipoprotein cholesterol (LDL-C and HDL-C), fasting blood sugar (FBS), insulin, S100B, S100A1 and ZAG protein were examined by enzymatic and ELISA laboratory methods. Homeostatic model assessment- insulin resistance (HOMA-IR) index was calculated. Results: Serum levels of S100B, S100A1 and ZAG were comparable between men and women groups. S100B protein was positively associated with TG (r= 0.41, p= 0.006), SBP (r= 0.46, p= 0.002), and DBP (r= 0.37, p= 0.02), but negatively with HDL-c in men. Serum levels of S100A1 were significantly and negatively correlated with WC (r= -0.33, p= 0.03), TG (r= -0.37, p= 0.01), insulin (r= -0.31, p= 0.04) and HOMA-IR (r= -0.32, p= 0.03), in women. -
Datasheet: VMA00595 Product Details
Datasheet: VMA00595 Description: MOUSE ANTI S100A8 Specificity: S100A8 Format: Purified Product Type: PrecisionAb™ Monoclonal Isotype: IgG2b Quantity: 100 µl Product Details Applications This product has been reported to work in the following applications. This information is derived from testing within our laboratories, peer-reviewed publications or personal communications from the originators. Please refer to references indicated for further information. For general protocol recommendations, please visit www.bio-rad-antibodies.com/protocols. Yes No Not Determined Suggested Dilution Western Blotting 1/1000 PrecisionAb antibodies have been extensively validated for the western blot application. The antibody has been validated at the suggested dilution. Where this product has not been tested for use in a particular technique this does not necessarily exclude its use in such procedures. Further optimization may be required dependant on sample type. Target Species Human Species Cross Reacts with: Mouse Reactivity N.B. Antibody reactivity and working conditions may vary between species. Product Form Purified IgG - liquid Preparation Mouse monoclonal antibody affinity purified on immunogen from tissue culture supernatant Buffer Solution Phosphate buffered saline Preservative 0.09% Sodium Azide (NaN3) Stabilisers 1% Bovine Serum Albumin Immunogen Full length recombinant human S100A8 External Database Links UniProt: P05109 Related reagents Entrez Gene: 6279 S100A8 Related reagents Synonyms CAGA, CFAG, MRP8 Page 1 of 2 Specificity Mouse anti Human S100A8 antibody recognizes S100A8, also known as MRP-8, S100 calcium- binding protein A8 (calgranulin A), calprotectin L1L subunit, leukocyte L1 complex light chain or migration inhibitory factor-related protein 8. The protein encoded by S100A8 is a member of the S100 family of proteins containing 2 EF-hand calcium-binding motifs. -
Dysfunctional Family Roles in an Effort to 1) Survive and 2) Have a Sense of Stability, the Family Members Will Usually Develop Specific Roles
Growing Up In a Dysfunctional Family “Dysfunctional simply means that it doesn’t work, but it often looks like it does. In contrast to a functional family, it has been suggested that the dysfunctional family is a dictatorship run by its sickest member. It is one that does not function in a normal, healthy way. The family members are unable to find stability. A dysfunctional family is characterized BY LACK OF BOUNDARIES. We usually think of alcoholism or drug addiction in the family as the primary cause of the dysfunction, but it can also be caused by a variety of other different problems that families face: a serious illness (such as cancer), a death in the family, or mental illness. It can be caused by either an extramarital affair, religious abuse, or other abuses. It can be caused by anything that rocks or stresses the family. Often dysfunction is intergenerational. (means that families pass on what they learn to the next generation and so on. .) The question is no longer, “Did I come from a dysfunctional family?”, but “To what degree was my family dysfunctional? It is not “How dysfunctional was my family?” but , “In what ways was it dysfunctional?” It is not “Did it affect me to come from this family?” but “How did it affect me, what roles did I play and what am I left with now?” It is not “Do I need to do something about my family of origin and the resulting boundary issues?” but “What do I do to address the specific issues resulting from my dysfunctional family of origin?”” O’Neil & Newbold Dysfunctional Family Roles In an effort to 1) survive and 2) have a sense of stability, the family members will usually develop specific roles. -
A Novel Computational Algorithm for Predicting Immune Cell Types Using Single-Cell RNA Sequencing Data
A novel computational algorithm for predicting immune cell types using single-cell RNA sequencing data By Shuo Jia A hesis submitted to the Faculty of Graduate Studies of The University of Manitoba n partial fulfillment of the requirements of the degree of MASTER OF SCIENCE Department of Biochemistry and Medical Genetics University of Manitoba Winnipeg, Manitoba, Canada Copyright © 2020 by Shuo Jia Abstract Background: Cells from our immune system detect and kill pathogens to protect our body against many diseases. However, current methods for determining cell types have some major limitations, such as being time-consuming and with low throughput rate, etc. These problems stack up and hinder the deep exploration of cellular heterogeneity. Immune cells that are associated with cancer tissues play a critical role in revealing the stages of tumor development. Identifying the immune composition within tumor microenvironments in a timely manner will be helpful to improve clinical prognosis and therapeutic management for cancer. Single-cell RNA sequencing (scRNA-seq), an RNA sequencing (RNA-seq) technique that focuses on a single cell level, has provided us with the ability to conduct cell type classification. Although unsupervised clustering approaches are the major methods for analyzing scRNA-seq datasets, their results vary among studies with different input parameters and sizes. However, in supervised machine learning methods, information loss and low prediction accuracy are the key limitations. Methods and Results: Genes in the human genome align to chromosomes in a particular order. Hence, we hypothesize incorporating this information into our model will potentially improve the cell type classification performance. In order to utilize gene positional information, we introduce chromosome-based neural network, namely ChrNet, a novel chromosome-specific re-trainable supervised learning method based on a one-dimensional 1 convolutional neural network (1D-CNN). -
Discovery of Endoplasmic Reticulum Calcium Stabilizers to Rescue ER-Stressed Podocytes in Nephrotic Syndrome
Discovery of endoplasmic reticulum calcium stabilizers to rescue ER-stressed podocytes in nephrotic syndrome Sun-Ji Parka, Yeawon Kima, Shyh-Ming Yangb, Mark J. Hendersonb, Wei Yangc, Maria Lindahld, Fumihiko Uranoe, and Ying Maggie Chena,1 aDivision of Nephrology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110; bNational Center for Advancing Translational Sciences, National Institutes of Health, Rockville, MD 20850; cDepartment of Genetics, Washington University School of Medicine, St. Louis, MO 63110; dInstitute of Biotechnology, University of Helsinki, Helsinki, Finland 00014; and eDivision of Endocrinology, Metabolism, and Lipid Research, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110 Edited by Martin R. Pollak, Beth Israel Deaconess Medical Center, Brookline, MA, and approved May 28, 2019 (received for review August 16, 2018) Emerging evidence has established primary nephrotic syndrome activating transcription factor 6 (ATF6), which act as proximal (NS), including focal segmental glomerulosclerosis (FSGS), as a sensors of ER stress. ER stress activates these sensors by inducing primary podocytopathy. Despite the underlying importance of phosphorylation and homodimerization of IRE1α and PERK/ podocyte endoplasmic reticulum (ER) stress in the pathogenesis of eukaryotic initiation factor 2α (eIF2α), as well as relocalization of NS, no treatment currently targets the podocyte ER. In our mono- ATF6 to the Golgi, where it is cleaved by S1P/S2P proteases from genic podocyte ER stress-induced NS/FSGS mouse model, the 90 kDa to the active 50-kDa ATF6 (8), leading to activation of podocyte type 2 ryanodine receptor (RyR2)/calcium release channel their respective downstream transcription factors, spliced XBP1 on the ER was phosphorylated, resulting in ER calcium leak and (XBP1s), ATF4, and p50ATF6 (8–10). -
Review Article S100 Protein Family in Human Cancer
Am J Cancer Res 2014;4(2):89-115 www.ajcr.us /ISSN:2156-6976/ajcr0000257 Review Article S100 protein family in human cancer Hongyan Chen, Chengshan Xu, Qing’e Jin, Zhihua Liu The State Key Laboratory of Molecular Oncology, Cancer Institute and Hospital, Chinese Academy of Medical Sci- ences and Peking Union Medical College, Beijing 100021, China Received January 16, 2014; Accepted February 10, 2014; Epub March 1, 2014; Published March 15, 2014 Abstract: S100 protein family has been implicated in multiple stages of tumorigenesis and progression. Among the S100 genes, 22 are clustered at chromosome locus 1q21, a region frequently rearranged in cancers. S100 protein possesses a wide range of intracellular and extracellular functions such as regulation of calcium homeostasis, cell proliferation, apoptosis, cell invasion and motility, cytoskeleton interactions, protein phosphorylation, regulation of transcriptional factors, autoimmunity, chemotaxis, inflammation and pluripotency. Many lines of evidence suggest that altered expression of S100 proteins was associated with tumor progression and prognosis. Therefore, S100 proteins might also represent potential tumor biomarkers and therapeutic targets. In this review, we summarize the evidence connecting S100 protein family and cancer and discuss the mechanisms by which S100 exerts its diverse functions. Keywords: S100 proteins, proliferation, apoptosis, invasion, migration, pluripotency, biomarker Introduction and their relationship with different cancers because of their involvement in a variety of bio- The S100 gene family is the largest subfamily logical events which are closely related to of calcium binding proteins of EF-hand type [1]. tumorigenesis and cancer progression. The To date, at least 25 distinct members of this association between S100 proteins and cancer subgroup have been described. -
By Jennifer M. Fogel a Dissertation Submitted in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy
A MODERN FAMILY: THE PERFORMANCE OF “FAMILY” AND FAMILIALISM IN CONTEMPORARY TELEVISION SERIES by Jennifer M. Fogel A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy (Communication) in The University of Michigan 2012 Doctoral Committee: Associate Professor Amanda D. Lotz, Chair Professor Susan J. Douglas Professor Regina Morantz-Sanchez Associate Professor Bambi L. Haggins, Arizona State University © Jennifer M. Fogel 2012 ACKNOWLEDGEMENTS I owe my deepest gratitude to the members of my dissertation committee – Dr. Susan J. Douglas, Dr. Bambi L. Haggins, and Dr. Regina Morantz-Sanchez, who each contributed their time, expertise, encouragement, and comments throughout this entire process. These women who have mentored and guided me for a number of years have my utmost respect for the work they continue to contribute to our field. I owe my deepest gratitude to my advisor Dr. Amanda D. Lotz, who patiently refused to accept anything but my best work, motivated me to be a better teacher and academic, praised my successes, and will forever remain a friend and mentor. Without her constructive criticism, brainstorming sessions, and matching appreciation for good television, I would have been lost to the wolves of academia. One does not make a journey like this alone, and it would be remiss of me not to express my humble thanks to my parents and sister, without whom seven long and lonely years would not have passed by so quickly. They were both my inspiration and staunchest supporters. Without their tireless encouragement, laughter, and nurturing this dissertation would not have been possible. -
Glial Protein S100B Modulates Long-Term Neuronal Synaptic Plasticity
Glial protein S100B modulates long-term neuronal synaptic plasticity Hiroshi Nishiyama*†, Thomas Kno¨ pfel†, Shogo Endo‡, and Shigeyoshi Itohara*§ *Laboratories for Behavioral Genetics and †Neuronal Circuit Dynamics, and ‡Neuronal Circuit Mechanisms Research Group, Brain Science Institute (BSI), Institute of Physical and Chemical Research (RIKEN), 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan Communicated by Richard F. Thompson, University of Southern California, Los Angeles, CA, January 11, 2002 (received for review August 1, 2001) Glial cells are traditionally regarded as elements for structural subject of debate (1). Transgenic mice overexpressing human support and ionic homeostasis, but have recently attracted atten- S100B exhibit impaired hippocampal LTP and spatial learning tion as putative integral elements of the machinery involved in (11). Transgenic mice overexpressing S100B might not be ap- synaptic transmission and plasticity. Here, we demonstrate that propriate for evaluating the physiological roles of S100B, how- calcium-binding protein S100B, which is synthesized in consider- ever, because overexpression of S100B partly mimics patholog- able amounts in astrocytes (a major glial cell subtype), modulates ical conditions in some neuronal diseases, such as Down’s long-term synaptic plasticity. Mutant mice devoid of S100B devel- syndrome and Alzheimer’s disease (12, 13). The constitutive oped normally and had no detectable abnormalities in the cyto- overexpression of S100B might cause chronic neuronal damage architecture of the brain. These mutant mice, however, had (14, 15). Thus, there is no clear consensus regarding the signif- strengthened synaptic plasticity as identified by enhanced long- icance of this glial protein in neuronal synaptic plasticity. term potentiation (LTP) in the hippocampal CA1 region. -
Tumor-Infiltrating Monocytes/Macrophages Promote Tumor Invasion and Migration by Upregulating S100A8 and S100A9 Expression in Ca
OPEN Oncogene (2016) 35, 5735–5745 © 2016 Macmillan Publishers Limited, part of Springer Nature. All rights reserved 0950-9232/16 www.nature.com/onc ORIGINAL ARTICLE Tumor-infiltrating monocytes/macrophages promote tumor invasion and migration by upregulating S100A8 and S100A9 expression in cancer cells SY Lim, AE Yuzhalin, AN Gordon-Weeks and RJ Muschel Myeloid cells promote the development of distant metastases, but little is known about the molecular mechanisms underlying this process. Here we have begun to uncover the effects of myeloid cells on cancer cells in a mouse model of liver metastasis. Monocytes/macrophages, but not granulocytes, isolated from experimental liver metastases stimulated migration and invasion of MC38 colon and Lewis lung carcinoma cells. In response to conditioned media from tumor-infiltrating monocytes/macrophages, cancer cells upregulated S100a8 and S100a9 messenger RNA expression through an extracellular signal-related kinase-dependent mechanism. Suppression of S100A8 and S100A9 in cancer cells using short hairpin RNA significantly diminished migration and invasion in culture. Downregulation of S100A8 and S100A9 had no effect on subcutaneous tumor growth. However, colony size was greatly reduced in liver metastases with decreased invasion into adjacent tissue. In tissue culture and in the liver colonies derived from cancer cells with knockdown of S100A8 and S100A9, MMP2 and MMP9 expression was decreased, consistent with the reduction in migration and invasion. Our findings demonstrate that monocytes/macrophages in the metastatic liver microenvironment induce S100A8 and S100A9 in cancer cells, and that these proteins are essential for tumor cell migration and invasion. S100A8 and S100A9, however, are not responsible for stimulation of proliferation. -
CCN3 and Calcium Signaling Alain Lombet1, Nathalie Planque2, Anne-Marie Bleau2, Chang Long Li2 and Bernard Perbal*2
Cell Communication and Signaling BioMed Central Review Open Access CCN3 and calcium signaling Alain Lombet1, Nathalie Planque2, Anne-Marie Bleau2, Chang Long Li2 and Bernard Perbal*2 Address: 1CNRS UMR 8078, Hôpital Marie Lannelongue, 133, Avenue de la Résistance 92350 Le PLESSIS-ROBINSON, France and 2Laboratoire d'Oncologie Virale et Moléculaire, Tour 54, Case 7048, Université Paris 7-D.Diderot, 2 Place Jussieu 75005 PARIS, France Email: Alain Lombet - [email protected]; Nathalie Planque - [email protected]; Anne-Marie Bleau - [email protected]; Chang Long Li - [email protected]; Bernard Perbal* - [email protected] * Corresponding author Published: 15 August 2003 Received: 26 June 2003 Accepted: 15 August 2003 Cell Communication and Signaling 2003, 1:1 This article is available from: http://www.biosignaling.com/content/1/1/1 © 2003 Lombet et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL. Abstract The CCN family of genes consists presently of six members in human (CCN1-6) also known as Cyr61 (Cystein rich 61), CTGF (Connective Tissue Growth Factor), NOV (Nephroblastoma Overexpressed gene), WISP-1, 2 and 3 (Wnt-1 Induced Secreted Proteins). Results obtained over the past decade have indicated that CCN proteins are matricellular proteins, which are involved in the regulation of various cellular functions, such as proliferation, differentiation, survival, adhesion and migration. The CCN proteins have recently emerged as regulatory factors involved in both internal and external cell signaling.