Supplemental Figure 1. Confirmation of Family Member IRF8 Variants by Sanger Sequencing
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Screening and Identification of Key Biomarkers in Clear Cell Renal Cell Carcinoma Based on Bioinformatics Analysis
bioRxiv preprint doi: https://doi.org/10.1101/2020.12.21.423889; this version posted December 23, 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 The copyright holder for this preprint (which was not certified by peer review) is the author/funder.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. Screening and identification of key biomarkers in clear cell renal cell carcinoma based on bioinformatics analysis Basavaraj Vastrad1, Chanabasayya Vastrad*2 , Iranna Kotturshetti 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics, Chanabasava Nilaya, Bharthinagar, Dharwad 580001, Karanataka, India. 3. Department of Ayurveda, Rajiv Gandhi Education Society`s Ayurvedic Medical College, Ron, Karnataka 562209, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India bioRxiv preprint doi: https://doi.org/10.1101/2020.12.21.423889; this version posted December 23, 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 The copyright holder for this preprint (which was not certified by peer review) is the author/funder.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. Abstract Clear cell renal cell carcinoma (ccRCC) is one of the most common types of malignancy of the urinary system. The pathogenesis and effective diagnosis of ccRCC have become popular topics for research in the previous decade. In the current study, an integrated bioinformatics analysis was performed to identify core genes associated in ccRCC. An expression dataset (GSE105261) was downloaded from the Gene Expression Omnibus database, and included 26 ccRCC and 9 normal kideny samples. Assessment of the microarray dataset led to the recognition of differentially expressed genes (DEGs), which was subsequently used for pathway and gene ontology (GO) enrichment analysis. -
Imm Catalog.Pdf
$ Gene Symbol A B 3 C 4 D 9 E 10 F 11 G 12 H 13 I 14 J. K 17 L 18 M 19 N 20 O. P 22 R 26 S 27 T 30 U 32 V. W. X. Y. Z 33 A ® ® Gene Symbol Gene ID Antibody Monoclonal Antibody Polyclonal MaxPab Full-length Protein Partial-length Protein Antibody Pair KIt siRNA/Chimera Gene Symbol Gene ID Antibody Monoclonal Antibody Polyclonal MaxPab Full-length Protein Partial-length Protein Antibody Pair KIt siRNA/Chimera A1CF 29974 ● ● ADAMTS13 11093 ● ● ● ● ● A2M 2 ● ● ● ● ● ● ADAMTS20 80070 ● AACS 65985 ● ● ● ADAMTS5 11096 ● ● ● AANAT 15 ● ● ADAMTS8 11095 ● ● ● ● AATF 26574 ● ● ● ● ● ADAMTSL2 9719 ● AATK 9625 ● ● ● ● ADAMTSL4 54507 ● ● ABCA1 19 ● ● ● ● ● ADAR 103 ● ● ABCA5 23461 ● ● ADARB1 104 ● ● ● ● ABCA7 10347 ● ADARB2 105 ● ABCB9 23457 ● ● ● ● ● ADAT1 23536 ● ● ABCC4 10257 ● ● ● ● ADAT2 134637 ● ● ABCC5 10057 ● ● ● ● ● ADAT3 113179 ● ● ● ABCC8 6833 ● ● ● ● ADCY10 55811 ● ● ABCD2 225 ● ADD1 118 ● ● ● ● ● ● ABCD4 5826 ● ● ● ADD3 120 ● ● ● ABCG1 9619 ● ● ● ● ● ADH5 128 ● ● ● ● ● ● ABL1 25 ● ● ADIPOQ 9370 ● ● ● ● ● ABL2 27 ● ● ● ● ● ADK 132 ● ● ● ● ● ABO 28 ● ● ADM 133 ● ● ● ABP1 26 ● ● ● ● ● ADNP 23394 ● ● ● ● ABR 29 ● ● ● ● ● ADORA1 134 ● ● ACAA2 10449 ● ● ● ● ADORA2A 135 ● ● ● ● ● ● ● ACAN 176 ● ● ● ● ● ● ADORA2B 136 ● ● ACE 1636 ● ● ● ● ADRA1A 148 ● ● ● ● ACE2 59272 ● ● ADRA1B 147 ● ● ACER2 340485 ● ADRA2A 150 ● ● ACHE 43 ● ● ● ● ● ● ADRB1 153 ● ● ACIN1 22985 ● ● ● ADRB2 154 ● ● ● ● ● ACOX1 51 ● ● ● ● ● ADRB3 155 ● ● ● ● ACP5 54 ● ● ● ● ● ● ● ADRBK1 156 ● ● ● ● ACSF2 80221 ● ● ADRM1 11047 ● ● ● ● ACSF3 197322 ● ● AEBP1 165 ● ● ● ● ACSL4 2182 ● -
Immuno-Oncology Panel 1
Immuno-Oncology panel 1 Gene Symbol Target protein name UniProt ID (& link) Modification* (56 analytes) ADA17 ADAM17 metalloprotease domain 17 P78536 *blanks mean the assay detects the ANXA1 Annexin A1 P04083 non-modified peptide sequence ANXA1 Annexin A1 P04083 ARG2 arginase, type II P78540 ATM Serine-protein kinase ATM, Ataxia telangiectasia mutated Q13315 pS2996 ATM Serine-protein kinase ATM, Ataxia telangiectasia mutated Q13315 ATM Serine-protein kinase ATM, Ataxia telangiectasia mutated Q13315 pS367 ATM Serine-protein kinase ATM, Ataxia telangiectasia mutated Q13315 C10orf54 / VISTA chromosome 10 open reading frame 54 Q9H7M9 CCL5 C-C motif chemokine ligand 5 P13501 CD14 CD14 molecule P08571 CD163 CD163 molecule Q86VB7 CD274 / PDL1 Programmed cell death 1 ligand 1 CD274 Q9NZQ7 CD33 CD33 molecule P20138 CD40/TNR5 tumor necrosis factor receptor superfamily member 5 P25942 CD40/TNR5 tumor necrosis factor receptor superfamily member 5 P25942 CD47 CD47 molecule Q08722 CD70 CD70 antigen P32970 CD74/HG2A CD74 molecule, major histocompatibility complex, class II invariant chain Q8SNA0 CEACAM8 carcinoembryonic antigen-related cell adhesion molecule 8 P31997 CX3CL1 C-X3-C motif chemokine ligand 1 P78423 CXCL10 C-X-C motif chemokine ligand 10 P02778 CXCL13 chemokine (C-X-C motif) ligand 13 O43927 ENTPD1 ectonucleoside triphosphate diphosphohydrolase 1 Q86VV3 FAS/TNR6 Fas (TNF receptor superfamily, member 6) P25445 pY291 FAS/TNR6 Fas (TNF receptor superfamily, member 6) P25445 GAPDH Glyceraldehyde-3-phosphate dehydrogenase P04406 HAVCR2 hepatitis -
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. -
Tools for Cell Therapy and Immunoregulation
RnDSy-lu-2945 Tools for Cell Therapy and Immunoregulation Target Cell TIM-4 SLAM/CD150 BTNL8 PD-L2/B7-DC B7-H1/PD-L1 (Human) Unknown PD-1 B7-1/CD80 TIM-1 SLAM/CD150 Receptor TIM Family SLAM Family Butyrophilins B7/CD28 Families T Cell Multiple Co-Signaling Molecules Co-stimulatory Co-inhibitory Ig Superfamily Regulate T Cell Activation Target Cell T Cell Target Cell T Cell B7-1/CD80 B7-H1/PD-L1 T cell activation requires two signals: 1) recognition of the antigenic peptide/ B7-1/CD80 B7-2/CD86 CTLA-4 major histocompatibility complex (MHC) by the T cell receptor (TCR) and 2) CD28 antigen-independent co-stimulation induced by interactions between B7-2/CD86 B7-H1/PD-L1 B7-1/CD80 co-signaling molecules expressed on target cells, such as antigen-presenting PD-L2/B7-DC PD-1 ICOS cells (APCs), and their T cell-expressed receptors. Engagement of the TCR in B7-H2/ICOS L 2Ig B7-H3 (Mouse) the absence of this second co-stimulatory signal typically results in T cell B7-H1/PD-L1 B7/CD28 Families 4Ig B7-H3 (Human) anergy or apoptosis. In addition, T cell activation can be negatively regulated Unknown Receptors by co-inhibitory molecules present on APCs. Therefore, integration of the 2Ig B7-H3 Unknown B7-H4 (Mouse) Receptors signals transduced by co-stimulatory and co-inhibitory molecules following TCR B7-H5 4Ig B7-H3 engagement directs the outcome and magnitude of a T cell response Unknown Ligand (Human) B7-H5 including the enhancement or suppression of T cell proliferation, B7-H7 Unknown Receptor differentiation, and/or cytokine secretion. -
Association Between C4, C4A, and C4B Copy Number Variations And
www.nature.com/scientificreports OPEN Association between C4, C4A, and C4B copy number variations and susceptibility to autoimmune Received: 17 June 2016 Accepted: 04 January 2017 diseases: a meta-analysis Published: 16 February 2017 Na Li1, Jun Zhang2, Dan Liao2, Lu Yang2, Yingxiong Wang1 & Shengping Hou2,3 Although several studies have investigated the association between C4, C4A, and C4B gene copy number variations (CNVs) and susceptibility to autoimmune diseases, the results remain inconsistency for those diseases. Thus, in this study, a comprehensive meta-analysis was conducted to assess the role of C4, C4A, and C4B CNVs in autoimmune diseases in different ethnic groups. A total of 16 case-control studies described in 12 articles (8663 cases and 11099 controls) were included in this study. The pooled analyses showed that a low C4 gene copy number (GCN) (<4) was treated as a significant risk factor (odds ratio [OR] = 1.46, 95% confidence interval [CI] = 1.19–1.78) for autoimmune diseases compared with a higher GCN (>4). The pooled statistical results revealed that low C4 (<4) and low C4A (<2) GCNs could be risk factors for systemic lupus erythematosus (SLE) in Caucasian populations. Additionally, the correlation between C4B CNVs and all type of autoimmune diseases could not be confirmed by the current meta-analysis (OR = 1.07, 95% CI = 0.93–1.24). These data suggest that deficiency or absence of C4 and C4A CNVs may cause susceptibility to SLE. The complement system, which is involved in both innate and adaptive immunity, is characterized by triggered-enzyme cascades activated by alternative, lectin or classical pathways1. -
Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model
Downloaded from http://www.jimmunol.org/ by guest on September 25, 2021 T + is online at: average * The Journal of Immunology , 34 of which you can access for free at: 2016; 197:1477-1488; Prepublished online 1 July from submission to initial decision 4 weeks from acceptance to publication 2016; doi: 10.4049/jimmunol.1600589 http://www.jimmunol.org/content/197/4/1477 Molecular Profile of Tumor-Specific CD8 Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A. Waugh, Sonia M. Leach, Brandon L. Moore, Tullia C. Bruno, Jonathan D. Buhrman and Jill E. Slansky J Immunol cites 95 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html http://www.jimmunol.org/content/suppl/2016/07/01/jimmunol.160058 9.DCSupplemental This article http://www.jimmunol.org/content/197/4/1477.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2016 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 25, 2021. The Journal of Immunology Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A. -
CD4 T-Cell Cytokines Synergize to Induce Proliferation of Malignant and Nonmalignant Innate Intraepithelial Lymphocytes
CD4 T-cell cytokines synergize to induce proliferation of malignant and nonmalignant innate intraepithelial lymphocytes Yvonne M. C. Kooy-Winkelaara, Dagmar Bouwera, George M. C. Janssenb, Allan Thompsona, Martijn H. Brugmana, Frederike Schmitza, Arnoud H. de Rub, Tom van Gilsc, Gerd Boumac, Jon J. van Rooda,1, Peter A. van Veelenb, M. Luisa Mearind, Chris J. Mulderc, Frits Koninga, and Jeroen van Bergena,1 aDepartment of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden 2333 ZA, The Netherlands; bCenter for Proteomics and Metabolomics, Leiden University Medical Center, Leiden 2333 ZA, The Netherlands; cDepartment of Gastroenterology and Hepatology, VU University Medical Center, Amsterdam 1081 HZ, The Netherlands; and dDepartment of Pediatrics, Leiden University Medical Center, Leiden 2333 ZA, The Netherlands Contributed by Jon J. van Rood, December 7, 2016 (sent for review January 6, 2016; reviewed by Georg Gasteiger and Bana Jabri) − Refractory celiac disease type II (RCDII) is a severe complication of lymphoma, because the Lin IELs expanded in RCDII often give celiac disease (CD) characterized by the presence of an enlarged rise to type I enteropathy-associated T-cell lymphoma (EATL). − clonal population of innate intraepithelial lymphocytes (IELs) lacking The main treatment goal in RCDII is to eliminate the Lin IEL − classical B-, T-, and natural killer (NK)-cell lineage markers (Lin IELs) population before its transformation into a high-grade lymphoma. in the duodenum. In ∼50% of patients with RCDII, these Lin−IELs Cladribine (2-CDA) is thought to be especially active against low- develop into a lymphoma for which no effective treatment is avail- grade malignancies with limited proliferative capacity, and reduces − able. -
Pan-KIR2DL NK-Receptor Antibodies and Their Use in Diagnostik and Therapy
(19) TZZ _ T (11) EP 2 287 195 A2 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.: 23.02.2011 Bulletin 2011/08 C07K 16/28 (2006.01) G01N 33/52 (2006.01) (21) Application number: 10178924.6 (22) Date of filing: 01.07.2005 (84) Designated Contracting States: • Romagne, François AT BE BG CH CY CZ DE DK EE ES FI FR GB GR 13600 La Ciotat (FR) HU IE IS IT LI LT LU LV MC NL PL PT RO SE SI • Wagtmann, Peter, Andreas, Nicolai, Reumert SK TR 2960 Rungsted Kyst (DK) • Svendsen, Ivan (30) Priority: 06.01.2005 DK 200500025 2765 Smorum (DK) 01.07.2004 PCT/DK2004/000470 • Zahn, Stefan 01.07.2004 PCT/IB2004/002464 2750 Ballerup (DK) • Svensson, Anders (62) Document number(s) of the earlier application(s) in 21746 Malmö (DK) accordance with Art. 76 EPC: • Thorolfsson, Matthias 05758642.2 / 1 791 868 2920 Charlottenlund (DK) • Berg Padkaer, Soren (71) Applicants: 3500 Vaerlose (DK) • Novo Nordisk A/S • Kjaergaard, Kristian 2880 Bagsvaerd (DK) 2750 Ballerup (DK) • Innate Pharma • Spee, Pieter 13009 Marseille (FR) 3450 Allerod (DK) • Universita di Genova • Wilken, Michael 16132 Genova (IT) 3390 Hundested (DK) (72) Inventors: (74) Representative: Gallois, Valérie et al • Moretta, Alessandro Cabinet BECKER & ASSOCIES 16133 Genova (IT) 25, rue Louis Le Grand • Della Chiesa, Mariella 75002 Paris (FR) 16132 Genova (IT) • Andre, Pascale Remarks: 13006 Marseille (FR) This application was filed on 23-09-2010 as a • Gauthier, Laurent divisional application to the application mentioned 13008 Marseille (FR) under INID code 62. -
WO 2016/147053 Al 22 September 2016 (22.09.2016) P O P C T
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2016/147053 Al 22 September 2016 (22.09.2016) P O P C T (51) International Patent Classification: (71) Applicant: RESVERLOGIX CORP. [CA/CA]; 300, A61K 31/551 (2006.01) A61P 37/02 (2006.01) 4820 Richard Road Sw, Calgary, AB, T3E 6L1 (CA). A61K 31/517 (2006.01) C07D 239/91 (2006.01) (72) Inventors: WASIAK, Sylwia; 431 Whispering Water (21) International Application Number: Trail, Calgary, AB, T3Z 3V1 (CA). KULIKOWSKI, PCT/IB20 16/000443 Ewelina, B.; 31100 Swift Creek Terrace, Calgary, AB, T3Z 0B7 (CA). HALLIDAY, Christopher, R.A.; 403 (22) International Filing Date: 138-18th Avenue SE, Calgary, AB, T2G 5P9 (CA). GIL- 10 March 2016 (10.03.2016) HAM, Dean; 249 Scenic View Close NW, Calgary, AB, (25) Filing Language: English T3L 1Y5 (CA). (26) Publication Language: English (81) Designated States (unless otherwise indicated, for every kind of national protection available): AE, AG, AL, AM, (30) Priority Data: AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, 62/132,572 13 March 2015 (13.03.2015) US BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, 62/264,768 8 December 2015 (08. 12.2015) US DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, [Continued on nextpage] (54) Title: COMPOSITIONS AND THERAPEUTIC METHODS FOR THE TREATMENT OF COMPLEMENT-ASSOCIATED DISEASES (57) Abstract: The invention comprises methods of modulating the complement cascade in a mammal and for treating and/or preventing diseases and disorders as sociated with the complement pathway by administering a compound of Formula I or Formula II, such as, for example, 2-(4-(2-hydroxyethoxy)-3,5-dimethylphenyl)- 5,7-dimethoxyquinazolin-4(3H)-one or a pharmaceutically acceptable salt thereof. -
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. -
Anti-C4B Monoclonal Antibody, Clone FQS3001(3) (DCABH-5883) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use
Anti-C4B monoclonal antibody, clone FQS3001(3) (DCABH-5883) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Product Overview Rabbit monoclonal to C4 Antigen Description This gene encodes the basic form of complement factor 4, part of the classical activation pathway. The protein is expressed as a single chain precursor which is proteolytically cleaved into a trimer of alpha, beta, and gamma chains prior to secretion. The trimer provides a surface for interaction between the antigen-antibody complex and other complement components. The alpha chain may be cleaved to release C4 anaphylatoxin, a mediator of local inflammation. Deficiency of this protein is associated with systemic lupus erythematosus. This gene localizes to the major histocompatibility complex (MHC) class III region on chromosome 6. Varying haplotypes of this gene cluster exist, such that individuals may have 1, 2, or 3 copies of this gene. In addition, this gene exists as a long form and a short form due to the presence or absence of a 6.4 kb endogenous HERV-K retrovirus in intron 9. This GeneID and its associated RefSeq record represent a second copy of C4B found on ALT_REF_LOCI_7. Immunogen Synthetic peptide within Human C4 aa 1200-1300 (Cysteine residue). The exact sequence is proprietary. Note: this sequence is identical in both C4 subunits A (P0C0L4) and B (P0C0L5).Database link: P0C0L4 Isotype IgG Source/Host Rabbit Species Reactivity Human Clone FQS3001(3) Purity Tissue culture supernatant Conjugate Unconjugated Applications WB, ICC/IF Positive Control HepG2 cell lysate, HepG2 cells Format Liquid Size 100 μl 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 1 © Creative Diagnostics All Rights Reserved Buffer pH: 7.20; Preservative: 0.01% Sodium azide; Constituents: 49% PBS, 50% Glycerol, 0.05% BSA Preservative 0.01% Sodium Azide Storage Store at +4°C short term (1-2 weeks).