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Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse
Welcome to More Choice CD Marker Handbook For more information, please visit: Human bdbiosciences.com/eu/go/humancdmarkers Mouse bdbiosciences.com/eu/go/mousecdmarkers Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse CD3 CD3 CD (cluster of differentiation) molecules are cell surface markers T Cell CD4 CD4 useful for the identification and characterization of leukocytes. The CD CD8 CD8 nomenclature was developed and is maintained through the HLDA (Human Leukocyte Differentiation Antigens) workshop started in 1982. CD45R/B220 CD19 CD19 The goal is to provide standardization of monoclonal antibodies to B Cell CD20 CD22 (B cell activation marker) human antigens across laboratories. To characterize or “workshop” the antibodies, multiple laboratories carry out blind analyses of antibodies. These results independently validate antibody specificity. CD11c CD11c Dendritic Cell CD123 CD123 While the CD nomenclature has been developed for use with human antigens, it is applied to corresponding mouse antigens as well as antigens from other species. However, the mouse and other species NK Cell CD56 CD335 (NKp46) antibodies are not tested by HLDA. Human CD markers were reviewed by the HLDA. New CD markers Stem Cell/ CD34 CD34 were established at the HLDA9 meeting held in Barcelona in 2010. For Precursor hematopoetic stem cell only hematopoetic stem cell only additional information and CD markers please visit www.hcdm.org. Macrophage/ CD14 CD11b/ Mac-1 Monocyte CD33 Ly-71 (F4/80) CD66b Granulocyte CD66b Gr-1/Ly6G Ly6C CD41 CD41 CD61 (Integrin b3) CD61 Platelet CD9 CD62 CD62P (activated platelets) CD235a CD235a Erythrocyte Ter-119 CD146 MECA-32 CD106 CD146 Endothelial Cell CD31 CD62E (activated endothelial cells) Epithelial Cell CD236 CD326 (EPCAM1) For Research Use Only. -
Viewed Under 23 (B) Or 203 (C) fi M M Male Cko Mice, and Largely Unaffected Magni Cation; Scale Bars, 500 M (B) and 50 M (C)
BRIEF COMMUNICATION www.jasn.org Renal Fanconi Syndrome and Hypophosphatemic Rickets in the Absence of Xenotropic and Polytropic Retroviral Receptor in the Nephron Camille Ansermet,* Matthias B. Moor,* Gabriel Centeno,* Muriel Auberson,* † † ‡ Dorothy Zhang Hu, Roland Baron, Svetlana Nikolaeva,* Barbara Haenzi,* | Natalya Katanaeva,* Ivan Gautschi,* Vladimir Katanaev,*§ Samuel Rotman, Robert Koesters,¶ †† Laurent Schild,* Sylvain Pradervand,** Olivier Bonny,* and Dmitri Firsov* BRIEF COMMUNICATION *Department of Pharmacology and Toxicology and **Genomic Technologies Facility, University of Lausanne, Lausanne, Switzerland; †Department of Oral Medicine, Infection, and Immunity, Harvard School of Dental Medicine, Boston, Massachusetts; ‡Institute of Evolutionary Physiology and Biochemistry, St. Petersburg, Russia; §School of Biomedicine, Far Eastern Federal University, Vladivostok, Russia; |Services of Pathology and ††Nephrology, Department of Medicine, University Hospital of Lausanne, Lausanne, Switzerland; and ¶Université Pierre et Marie Curie, Paris, France ABSTRACT Tight control of extracellular and intracellular inorganic phosphate (Pi) levels is crit- leaves.4 Most recently, Legati et al. have ical to most biochemical and physiologic processes. Urinary Pi is freely filtered at the shown an association between genetic kidney glomerulus and is reabsorbed in the renal tubule by the action of the apical polymorphisms in Xpr1 and primary fa- sodium-dependent phosphate transporters, NaPi-IIa/NaPi-IIc/Pit2. However, the milial brain calcification disorder.5 How- molecular identity of the protein(s) participating in the basolateral Pi efflux remains ever, the role of XPR1 in the maintenance unknown. Evidence has suggested that xenotropic and polytropic retroviral recep- of Pi homeostasis remains unknown. Here, tor 1 (XPR1) might be involved in this process. Here, we show that conditional in- we addressed this issue in mice deficient for activation of Xpr1 in the renal tubule in mice resulted in impaired renal Pi Xpr1 in the nephron. -
ACTL6A Promotes the Proliferation of Esophageal Squamous Cell Carcinoma Cells and Correlates with Poor Clinical Outcomes
OncoTargets and Therapy Dovepress open access to scientific and medical research Open Access Full Text Article ORIGINAL RESEARCH ACTL6A Promotes the Proliferation of Esophageal Squamous Cell Carcinoma Cells and Correlates with Poor Clinical Outcomes This article was published in the following Dove Press journal: OncoTargets and Therapy Rui-zhe Li1 Background: ACTL6A, a regulatory subunit of ATP-dependent chromatin-remodeling Yun-yun Li1,2 complexes SWI/SNF, has been identified as a central oncogenic driver in many tumor types. Hui Qin1 Materials and Methods: We used immunohistochemistry (IHC) to detect ACTL6A Shan-shan Li1 expression in esophageal squamous cell carcinoma (ESCC) tissues. Then, the effect of ACTL6A on proliferation and DNA synthesis was explored by using cell counting kit 8 1 Department of Pathology, School of (CCK8) and EdU retention assays. The potential oncogenic mechanism of ACTL6A in Basic Medical Sciences, Zhengzhou University and First Affiliated Hospital of ESCC cells was also analyzed by flow cytometry and Western blotting. We further estab Zhengzhou University, Zhengzhou, lished an ESCC xenograft mouse model to validate the in vitro results. Henan 450000, People’s Republic of China; 2Department of Stomatology, First Results: ACTL6A expression, localized in cancer cell nuclei, was markedly higher in ESCC Affiliated Hospital of Zhengzhou tissues than in the corresponding noncancerous tissues (P<0.001) and was positively asso University, Zhengzhou, Henan 450000, ciated with tumor size, histological differentiation, T stage and tumor-node-metastasis People’s Republic of China (TNM) stage. Kaplan–Meier analysis revealed that high ACTL6A expression was signifi cantly associated with poor overall survival (OS) (P = 0.008, HR= 2.562, 95% CI: 1.241– 5.289), and decision curve analysis (DCA) demonstrated that ACTL6A could increase the clinical prognostic efficiency of the original clinical prediction model. -
Supplemental Table S1
Entrez Gene Symbol Gene Name Affymetrix EST Glomchip SAGE Stanford Literature HPA confirmed Gene ID Profiling profiling Profiling Profiling array profiling confirmed 1 2 A2M alpha-2-macroglobulin 0 0 0 1 0 2 10347 ABCA7 ATP-binding cassette, sub-family A (ABC1), member 7 1 0 0 0 0 3 10350 ABCA9 ATP-binding cassette, sub-family A (ABC1), member 9 1 0 0 0 0 4 10057 ABCC5 ATP-binding cassette, sub-family C (CFTR/MRP), member 5 1 0 0 0 0 5 10060 ABCC9 ATP-binding cassette, sub-family C (CFTR/MRP), member 9 1 0 0 0 0 6 79575 ABHD8 abhydrolase domain containing 8 1 0 0 0 0 7 51225 ABI3 ABI gene family, member 3 1 0 1 0 0 8 29 ABR active BCR-related gene 1 0 0 0 0 9 25841 ABTB2 ankyrin repeat and BTB (POZ) domain containing 2 1 0 1 0 0 10 30 ACAA1 acetyl-Coenzyme A acyltransferase 1 (peroxisomal 3-oxoacyl-Coenzyme A thiol 0 1 0 0 0 11 43 ACHE acetylcholinesterase (Yt blood group) 1 0 0 0 0 12 58 ACTA1 actin, alpha 1, skeletal muscle 0 1 0 0 0 13 60 ACTB actin, beta 01000 1 14 71 ACTG1 actin, gamma 1 0 1 0 0 0 15 81 ACTN4 actinin, alpha 4 0 0 1 1 1 10700177 16 10096 ACTR3 ARP3 actin-related protein 3 homolog (yeast) 0 1 0 0 0 17 94 ACVRL1 activin A receptor type II-like 1 1 0 1 0 0 18 8038 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 1 0 0 0 0 19 8751 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 1 0 0 0 0 20 8728 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 1 0 0 0 0 21 81792 ADAMTS12 ADAM metallopeptidase with thrombospondin type 1 motif, 12 1 0 0 0 0 22 9507 ADAMTS4 ADAM metallopeptidase with thrombospondin type 1 -
Beta-Arrestin-Mediated Signaling in the Heart
SPECIAL ARTICLE Circ J 2008; 72: 1725–1729 Beta-Arrestin-Mediated Signaling in the Heart Priyesh A. Patel, BS; Douglas G. Tilley, PhD*; Howard A. Rockman, MD*,** Beta-arrestin is a multifunctional adapter protein well known for its role in G-protein-coupled receptor (GPCR) desensitization. Exciting new evidence indicates thatβ-arrestin is also a signaling molecule capable of initiating its own G-protein-independent signaling at GPCRs. One of the best-studiedβ-arrestin signaling pathways is the one involvingβ-arrestin-dependent activation of a mitogen-activated protein kinase cascade, the extracellular regulated kinase (ERK). ERK signaling, which is classically activated by agonist stimulation of the epidermal growth factor receptor (EGFR), can be activated by a number of GPCRs in aβ-arrestin-dependent manner. Recent work in animal models of heart failure suggests thatβ-arrestin-dependent activation of EGFR/ERK signaling by theβ-1-adrenergic receptor, and possibly the angiotensin II Type 1A receptor, are cardioprotective. Hence, a new model of signaling at cardiac GPCRs has emerged and implicates classical G-protein-mediated signaling with promoting harmful remodeling in heart failure, while concurrently linkingβ-arrestin-dependent, G-protein-inde- pendent signaling with cardioprotective effects. Based on this paradigm, a new class of drugs could be identified, termed “biased ligands”, which simultaneously block harmful G-protein signaling, while also promoting cardio- protectiveβ-arrestin-dependent signaling, leading to a potential breakthrough -
BMC Evolutionary Biology Biomed Central
BMC Evolutionary Biology BioMed Central Research article Open Access On the origins of arrestin and rhodopsin Carlos E Alvarez1,2,3 Address: 1Center for Molecular and Human Genetics, The Research Institute at Nationwide Children's Hospital, Columbus, OH, 43205, USA, 2Department of Pediatrics, The Ohio State University College of Medicine, Columbus, OH, 43210, USA and 3Novartis Institutes of BioMedical Research, CH-4002 Basel, Switzerland Email: Carlos E Alvarez - [email protected] Published: 29 July 2008 Received: 11 January 2008 Accepted: 29 July 2008 BMC Evolutionary Biology 2008, 8:222 doi:10.1186/1471-2148-8-222 This article is available from: http://www.biomedcentral.com/1471-2148/8/222 © 2008 Alvarez; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: G protein coupled receptors (GPCRs) are the most numerous proteins in mammalian genomes, and the most common targets of clinical drugs. However, their evolution remains enigmatic. GPCRs are intimately associated with trimeric G proteins, G protein receptor kinases, and arrestins. We conducted phylogenetic studies to reconstruct the history of arrestins. Those findings, in turn, led us to investigate the origin of the photosensory GPCR rhodopsin. Results: We found that the arrestin clan is comprised of the Spo0M protein family in archaea and bacteria, and the arrestin and Vps26 families in eukaryotes. The previously known animal arrestins are members of the visual/beta subfamily, which branched from the founding "alpha" arrestins relatively recently. -
ANKRD11 Gene Ankyrin Repeat Domain 11
ANKRD11 gene ankyrin repeat domain 11 Normal Function The ANKRD11 gene provides instructions for making a protein called ankyrin repeat domain 11 (ANKRD11). As its name suggests, this protein contains multiple regions called ankyrin domains; proteins with these domains help other proteins interact with each other. The ANKRD11 protein interacts with certain proteins called histone deacetylases, which are important for controlling gene activity. Through these interactions, ANKRD11 affects when genes are turned on and off. For example, ANKRD11 brings together histone deacetylases and other proteins called p160 coactivators. This association regulates the ability of p160 coactivators to turn on gene activity. ANKRD11 may also enhance the activity of a protein called p53, which controls the growth and division (proliferation) and the self-destruction (apoptosis) of cells. The ANKRD11 protein is found in nerve cells (neurons) in the brain. During embryonic development, ANKRD11 helps regulate the proliferation of these cells and development of the brain. Researchers speculate that the protein may also be involved in the ability of neurons to change and adapt over time (plasticity), which is important for learning and memory. ANKRD11 may function in other cells in the body and appears to be involved in normal bone development. Health Conditions Related to Genetic Changes KBG syndrome Several ANKRD11 gene mutations have been found to cause KBG syndrome, a condition characterized by large upper front teeth and other unusual facial features, skeletal abnormalities, and intellectual disability. Most of these mutations lead to an abnormally short ANKRD11 protein, which likely has little or no function. Reduction of this protein's function is thought to underlie the signs and symptoms of the condition. -
Molecular Mechanisms Underlying Noncoding Risk Variations in Psychiatric Genetic Studies
OPEN Molecular Psychiatry (2017) 22, 497–511 www.nature.com/mp REVIEW Molecular mechanisms underlying noncoding risk variations in psychiatric genetic studies X Xiao1,2, H Chang1,2 and M Li1 Recent large-scale genetic approaches such as genome-wide association studies have allowed the identification of common genetic variations that contribute to risk architectures of psychiatric disorders. However, most of these susceptibility variants are located in noncoding genomic regions that usually span multiple genes. As a result, pinpointing the precise variant(s) and biological mechanisms accounting for the risk remains challenging. By reviewing recent progresses in genetics, functional genomics and neurobiology of psychiatric disorders, as well as gene expression analyses of brain tissues, here we propose a roadmap to characterize the roles of noncoding risk loci in the pathogenesis of psychiatric illnesses (that is, identifying the underlying molecular mechanisms explaining the genetic risk conferred by those genomic loci, and recognizing putative functional causative variants). This roadmap involves integration of transcriptomic data, epidemiological and bioinformatic methods, as well as in vitro and in vivo experimental approaches. These tools will promote the translation of genetic discoveries to physiological mechanisms, and ultimately guide the development of preventive, therapeutic and prognostic measures for psychiatric disorders. Molecular Psychiatry (2017) 22, 497–511; doi:10.1038/mp.2016.241; published online 3 January 2017 RECENT GENETIC ANALYSES OF NEUROPSYCHIATRIC neurodevelopment and brain function. For example, GRM3, DISORDERS GRIN2A, SRR and GRIA1 were known to involve in the neuro- Schizophrenia, bipolar disorder, major depressive disorder and transmission mediated by glutamate signaling and synaptic autism are highly prevalent complex neuropsychiatric diseases plasticity. -
Implicating Gene and Cell Networks Responsible for Differential COVID
bioRxiv preprint doi: https://doi.org/10.1101/2021.06.07.447287; this version posted June 16, 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-NC 4.0 International license. 1 Implicating Gene and Cell Networks Responsible for 2 Differential COVID-19 Host Responses via an Interactive 3 Single Cell Web Portal 4 5 Kang Jin1,2, Eric E. Bardes1, Alexis Mitelpunkt1,3,4, Jake Y. Wang1, Surbhi Bhatnagar1,5, 6 Soma Sengupta6, Daniel Pomeranz Krummel6, Marc E. Rothenberg7, Bruce J. 7 Aronow1,8,9,* 8 9 1Division oF Biomedical InFormatics, Cincinnati Children's Hospital Medical Center, 10 Cincinnati, OH, 45229, USA 11 2Department oF Biomedical InFormatics, University oF Cincinnati, Cincinnati, OH, 45229, 12 USA 13 3Pediatric Rehabilitation, Dana-Dwek Children's Hospital, Tel Aviv Medical Center, Tel 14 Aviv, 6423906, Israel 15 4Sackler Faculty oF Medicine, Tel Aviv University, Tel Aviv, 6997801, Israel 16 5Department oF Electrical Engineering and Computer Science, University oF Cincinnati, 17 Cincinnati, OH, 45221, USA 18 6Department oF Neurology and Rehabilitation Medicine, University oF Cincinnati College 19 oF Medicine, Cincinnati, OH, 45267, USA. 20 7Division oF Allergy and Immunology, Department oF Pediatrics, Cincinnati Children's 21 Hospital Medical Center, University oF Cincinnati, Cincinnati, OH, 45229, USA 22 8Department oF Pediatrics, University oF Cincinnati School oF Medicine, Cincinnati, OH, 23 45256, USA 24 9Lead contact 25 *Correspondence: [email protected] (B.A.) 26 27 28 29 30 31 1 bioRxiv preprint doi: https://doi.org/10.1101/2021.06.07.447287; this version posted June 16, 2021. -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
Increased ACTL6A Occupancy Within Mswi/SNF Chromatin Remodelers
bioRxiv preprint doi: https://doi.org/10.1101/2021.03.22.435873; this version posted March 22, 2021. 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. Increased ACTL6A Occupancy Within mSWI/SNF Chromatin Remodelers Drives Human Squamous Cell Carcinoma Chiung-Ying Chang1,2,7, Zohar Shipony3,7, Ann Kuo1,2, Kyle M. Loh4,5, William J. Greenleaf3,6, Gerald R. Crabtree1,2,5* 1Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California 94305, USA. 2Department of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA. 3Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA. 4Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California 94305, USA. 5Department of Developmental Biology, Stanford University School of Medicine, Stanford, California 94305, USA. 6Department of Applied Physics, Stanford University, Stanford, California 94305, USA. 7These authors contributed equally. *Corresponding author: Gerald R. Crabtree, [email protected] Summary Mammalian SWI/SNF (BAF) chromatin remodelers play dosage-sensitive roles in many human malignancies and neurologic disorders. The gene encoding the BAF subunit, ACTL6A, is amplified at an early stage in the development of squamous cell carcinomas (SCCs), but its oncogenic role remains unclear. Here we demonstrate that ACTL6A overexpression leads to its stoichiometric assembly into BAF complexes and drives its interaction and engagement with specific regulatory regions in the genome. In normal epithelial cells, ACTL6A was sub-stoichiometric to other BAF subunits. However, increased ACTL6A levels by ectopic expression or in SCC cells led to near-saturation of ACTL6A within BAF complexes. -
Supplementary Table 1: Adhesion Genes Data Set
Supplementary Table 1: Adhesion genes data set PROBE Entrez Gene ID Celera Gene ID Gene_Symbol Gene_Name 160832 1 hCG201364.3 A1BG alpha-1-B glycoprotein 223658 1 hCG201364.3 A1BG alpha-1-B glycoprotein 212988 102 hCG40040.3 ADAM10 ADAM metallopeptidase domain 10 133411 4185 hCG28232.2 ADAM11 ADAM metallopeptidase domain 11 110695 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 195222 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 165344 8751 hCG20021.3 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 189065 6868 null ADAM17 ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme) 108119 8728 hCG15398.4 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 117763 8748 hCG20675.3 ADAM20 ADAM metallopeptidase domain 20 126448 8747 hCG1785634.2 ADAM21 ADAM metallopeptidase domain 21 208981 8747 hCG1785634.2|hCG2042897 ADAM21 ADAM metallopeptidase domain 21 180903 53616 hCG17212.4 ADAM22 ADAM metallopeptidase domain 22 177272 8745 hCG1811623.1 ADAM23 ADAM metallopeptidase domain 23 102384 10863 hCG1818505.1 ADAM28 ADAM metallopeptidase domain 28 119968 11086 hCG1786734.2 ADAM29 ADAM metallopeptidase domain 29 205542 11085 hCG1997196.1 ADAM30 ADAM metallopeptidase domain 30 148417 80332 hCG39255.4 ADAM33 ADAM metallopeptidase domain 33 140492 8756 hCG1789002.2 ADAM7 ADAM metallopeptidase domain 7 122603 101 hCG1816947.1 ADAM8 ADAM metallopeptidase domain 8 183965 8754 hCG1996391 ADAM9 ADAM metallopeptidase domain 9 (meltrin gamma) 129974 27299 hCG15447.3 ADAMDEC1 ADAM-like,