Supporting Information for Proteomics DOI 10.1002/Prca.200780101
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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. -
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. -
Remote Ischemic Preconditioning (RIPC) Modifies Plasma Proteome in Humans
Remote Ischemic Preconditioning (RIPC) Modifies Plasma Proteome in Humans Michele Hepponstall1,2,3,4, Vera Ignjatovic1,3, Steve Binos4, Paul Monagle1,3, Bryn Jones1,2, Michael H. H. Cheung1,2,3, Yves d’Udekem1,2, Igor E. Konstantinov1,2,3* 1 Haematology Research, Murdoch Childrens Research Institute; Melbourne, Victoria, Australia, 2 Cardiac Surgery Unit and Cardiology, Royal Children’s Hospital; Melbourne, Victoria, Australia, 3 Department of Paediatrics, The University of Melbourne; Melbourne, Victoria, Australia, 4 Bioscience Research Division, Department of Primary Industries, Melbourne, Victoria, Australia Abstract Remote Ischemic Preconditioning (RIPC) induced by brief episodes of ischemia of the limb protects against multi-organ damage by ischemia-reperfusion (IR). Although it has been demonstrated that RIPC affects gene expression, the proteomic response to RIPC has not been determined. This study aimed to examine RIPC induced changes in the plasma proteome. Five healthy adult volunteers had 4 cycles of 5 min ischemia alternating with 5 min reperfusion of the forearm. Blood samples were taken from the ipsilateral arm prior to first ischaemia, immediately after each episode of ischemia as well as, at 15 min and 24 h after the last episode of ischemia. Plasma samples from five individuals were analysed using two complementary techniques. Individual samples were analysed using 2Dimensional Difference in gel electrophoresis (2D DIGE) and mass spectrometry (MS). Pooled samples for each of the time-points underwent trypsin digestion and peptides generated were analysed in triplicate using Liquid Chromatography and MS (LC-MS). Six proteins changed in response to RIPC using 2D DIGE analysis, while 48 proteins were found to be differentially regulated using LC-MS. -
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). -
Pancancer Progression Human Vjune2017
Gene Symbol Accession Alias/Prev Symbol Official Full Name AAMP NM_001087.3 - angio-associated, migratory cell protein ABI3BP NM_015429.3 NESHBP|TARSH ABI family, member 3 (NESH) binding protein ACHE NM_000665.3 ACEE|ARACHE|N-ACHE|YT acetylcholinesterase ACTG2 NM_001615.3 ACT|ACTA3|ACTE|ACTL3|ACTSG actin, gamma 2, smooth muscle, enteric ACVR1 NM_001105.2 ACTRI|ACVR1A|ACVRLK2|ALK2|FOP|SKR1|TSRI activin A receptor, type I ACVR1C NM_145259.2 ACVRLK7|ALK7 activin A receptor, type IC ACVRL1 NM_000020.1 ACVRLK1|ALK-1|ALK1|HHT|HHT2|ORW2|SKR3|TSR-I activin A receptor type II-like 1 ADAM15 NM_207195.1 MDC15 ADAM metallopeptidase domain 15 ADAM17 NM_003183.4 ADAM18|CD156B|CSVP|NISBD|TACE ADAM metallopeptidase domain 17 ADAM28 NM_014265.4 ADAM 28|ADAM23|MDC-L|MDC-Lm|MDC-Ls|MDCL|eMDC II|eMDCII ADAM metallopeptidase domain 28 ADAM8 NM_001109.4 CD156|MS2 ADAM metallopeptidase domain 8 ADAM9 NM_001005845.1 CORD9|MCMP|MDC9|Mltng ADAM metallopeptidase domain 9 ADAMTS1 NM_006988.3 C3-C5|METH1 ADAM metallopeptidase with thrombospondin type 1 motif, 1 ADAMTS12 NM_030955.2 PRO4389 ADAM metallopeptidase with thrombospondin type 1 motif, 12 ADAMTS8 NM_007037.4 ADAM-TS8|METH2 ADAM metallopeptidase with thrombospondin type 1 motif, 8 ADAP1 NM_006869.2 CENTA1|GCS1L|p42IP4 ArfGAP with dual PH domains 1 ADD1 NM_001119.4 ADDA adducin 1 (alpha) ADM2 NM_001253845.1 AM2|dJ579N16.4 adrenomedullin 2 ADRA2B NM_000682.4 ADRA2L1|ADRA2RL1|ADRARL1|ALPHA2BAR|alpha-2BAR adrenoceptor alpha 2B AEBP1 NM_001129.3 ACLP AE binding protein 1 AGGF1 NM_018046.3 GPATC7|GPATCH7|HSU84971|HUS84971|VG5Q -
Apolipoprotein H, an Acute Phase Protein, a Performing Tool for Ultra-Sensitive Detection and Isolation of Microorganisms from Different Origins
2 Apolipoprotein H, an Acute Phase Protein, a Performing Tool for Ultra-Sensitive Detection and Isolation of Microorganisms from Different Origins Ilias Stefas1, Gregor Dubois2, Sylvia Tigrett1, Estelle Lucarz1 and Francisco Veas2 1ApoH-Technologies Faculty of Pharmacy, University Montpellier 1, Av Charles Flahault, Montpellier 2Comparative Molecular Immuno-Physiopathology Lab. UMR-MD3 Faculty of Pharmacy, University Montpellier 1, Av Charles Flahault, Montpellier France 1. Introduction Apolipoprotein H (ApoH), also known as beta2-glycoprotein I (ß2-GPI), is a plasma glycoprotein of 50 kDa. ApoH is present in human plasma at a concentration of between 150 and 300 mg/ml (Bouma et al., 1999). In blood, ApoH circulate in free conformations or bound to lipoproteins: chylomicrons, very low-density lipoprotein (VLDL), low density lipoprotein (LDL) and high-density lipoprotein (HDL). In addition, ApoH has a high affinity for triglyceride-rich lipoproteins. The amount of ApoH associated with plasma lipoproteins in healthy individuals varies according to the authors from 4 to 13% (Gambino et al., 1999a) up to about 40% (Polz & Kostner, 1979). ApoH is able to activate lipoprotein lipases (Lee et al., 1983). ApoH was isolated from the fraction of plasma lipoproteins, and described for the first time in 1961 by H. Schultze E (Schultze, 1961). In a lesser extent, ApoH is also associated to ß2-globulin fraction. ApoH is expressed in human liver, in intestinal cells and tissues (Averna et al., 1997). In rats, other sites of synthesis in low concentrations were identified as the kidney, small intestine, brain, cardiomyocytes of the heart, and at even lower in the spleen, stomach and prostate (Ragusa et al., 2006). -
Pathophysiological Mechanisms in Antiphospholipid Syndrome
Review Pathophysiological mechanisms in antiphospholipid syndrome Antiphospholipid syndrome is a systemic autoimmune disease associated with thrombosis and recurrent fetal loss in the setting of detectable antiphospholipid (aPL) antibodies. The major antigenic target has been identified as b2-glycoprotein I (b2GPI), which mediates binding of aPL antibodies to target cells including endothelial cells, monocytes, platelets and trophoblasts, leading to prothrombotic and proinflammatory changes that ultimately result in thrombosis and fetal loss. This article summarizes recent insights into the role of b2GPI in normal hemostasis, interactions between aPL antibodies, b2GPI and cell- surface molecules, molecular prothrombotic and proinflammatory changes induced by aPL antibodies and pathogenic changes leading to fetal loss in antiphospholipid syndrome. New directions in therapy using these insights are examined. 1 n n Brock E Harper , KEYWORDS: annexin anti-b2-glycoprotein I antibody antiphospholipid antibodies n antiphospholipid syndrome n endothelial cell activation n pathogenesis n platelet Rohan Willis1 activation n pregnancy loss n thrombosis n treatment & Silvia S Pierangeli†1 1Department of Internal Medicine, Division of Rheumatology, University Antiphospholipid syndrome (APS) is a systemic and use of hormone-replacement therapy or oral of Texas Medical Branch, Galveston, autoimmune disease characterized by recurrent contraceptives [9]. By contrast, venous thrombo- TX, USA †Author for correspondence: thrombosis and fetal loss in the presence of per- sis was associated with presence of hypertriglyc- [email protected] sistently positive antiphospholipid (aPL) antibod- eridemia, presence of a hereditary thrombophilia ies (Abs) including lupus anticoagulant (LAC), or aCL IgG more than 40 IU [9]. IgG/IgM anticardiolipin (aCL) Abs and anti-b2- Antiphospholipid syndrome causes significant glycoprotein I (b2GPI) Abs [1–3]. -
Review Article Mouse Homologues of Human Hereditary Disease
I Med Genet 1994;31:1-19 I Review article J Med Genet: first published as 10.1136/jmg.31.1.1 on 1 January 1994. Downloaded from Mouse homologues of human hereditary disease A G Searle, J H Edwards, J G Hall Abstract involve homologous loci. In this respect our Details are given of 214 loci known to be genetic knowledge of the laboratory mouse associated with human hereditary dis- outstrips that for all other non-human mam- ease, which have been mapped on both mals. The 829 loci recently assigned to both human and mouse chromosomes. Forty human and mouse chromosomes3 has now two of these have pathological variants in risen to 900, well above comparable figures for both species; in general the mouse vari- other laboratory or farm animals. In a previous ants are similar in their effects to the publication,4 102 loci were listed which were corresponding human ones, but excep- associated with specific human disease, had tions include the Dmd/DMD and Hprt/ mouse homologues, and had been located in HPRT mutations which cause little, if both species. The number has now more than any, harm in mice. Possible reasons for doubled (table 1A). Of particular interest are phenotypic differences are discussed. In those which have pathological variants in both most pathological variants the gene pro- the mouse and humans: these are listed in table duct seems to be absent or greatly 2. Many other pathological mutations have reduced in both species. The extensive been detected and located in the mouse; about data on conserved segments between half these appear to lie in conserved chromo- human and mouse chromosomes are somal segments. -
Assessing Changes in Biomarkers of Effect in Smokers Who Switch to a Closed System Electronic Cigarette
Assessing Changes In Biomarkers Of Effect In Smokers Who Switch To A Closed System Electronic Cigarette Liz Mason | Kunming, China | 26th October 2018 CONTENT 1. Background Biomarkers of exposure and effect Study Aim 2. 5-day Study Study design Results 3. Two-year study Study design Results 4. Summary Study Conclusions Background 5-day Study Two year study Conclusions 2 | VAPOUR PRODUCTS HAVE BEEN SHOWN TO REDUCE BIOMARKERS OF EXPOSURE Previous studies have demonstrated that when a smoker switches to a vapour product, they are exposed to significantly lower levels of carcinogens and toxicants in the aerosol... Reduced formation of toxicants in blu™ e-cigarette …and significant reductions in biomarkers of exposure… aerosol vs. conventional cigarette smoke “Chemical Composition of myblu™ Pod-System E-Cigarette Aerosols: A Quantitative Comparison with Conventional Cigarette Smoke”, Poster presentation, 1st Scientific Summit Tobacco Harm Reduction (http://www.fontemscience.com/wp-content/uploads/2018/06/2018-04-18-aerosol-chemistry-thr-summit-2018-poster_final.pdf); Tayyarah R and Long GA. “Comparison of select analytes in aerosol from e-cigarettes with smoke from conventional cigarettes and with ambient air.” Regulatory toxicology and pharmacology 70 3 (2014). O’Connell et al (2016): Reductions in biomarkers of exposure (BoE) to harmful or potentially harmful constituents (HPHCs) following partial or complete substitution of cigarettes with electronic cigarettes in adult smokers, Toxicology Mechanisms and Methods, DOI: 10.1080/15376516.2016.1196282. http://www.fontemscience.com/wp-content/uploads/2017/05/fontem2research-1.pdf Background 5-day Study Two year study Conclusions 3 | VAPOUR PRODUCTS HAVE BEEN SHOWN TO REDUCE BIOMARKERS OF EXPOSURE What is the biological impact when a smoker switches to a vapour product? Clinical markers: • can be defined as a measurable biochemical, physiologic, behavioural, or other alteration in an organism. -
Supplementary Table 1: List of the 316 Genes Regulated During Hyperglycemic Euinsulinemic Clamp in Skeletal Muscle
Supplementary Table 1: List of the 316 genes regulated during hyperglycemic euinsulinemic clamp in skeletal muscle. UGCluster Name Symbol Fold Change Cytoband Response to stress Hs.517581 Heme oxygenase (decycling) 1 HMOX1 3.80 22q12 Hs.374950 Metallothionein 1X MT1X 2.20 16q13 Hs.460867 Metallothionein 1B (functional) MT1B 1.70 16q13 Hs.148778 Oxidation resistance 1 OXR1 1.60 8q23 Hs.513626 Metallothionein 1F (functional) MT1F 1.47 16q13 Hs.534330 Metallothionein 2A MT2A 1.45 16q13 Hs.438462 Metallothionein 1H MT1H 1.42 16q13 Hs.523836 Glutathione S-transferase pi GSTP1 -1.74 11q13 Hs.459952 Stannin SNN -1.92 16p13 Immune response, cytokines & related Hs.478275 TNF (ligand) superfamily, member 10 (TRAIL) TNFSF10 1.58 3q26 Hs.278573 CD59 antigen p18-20 (protectin) CD59 1.49 11p13 Hs.534847 Complement component 4B, telomeric C4A 1.47 6p21.3 Hs.535668 Immunoglobulin lambda variable 6-57 IGLV6-57 1.40 22q11.2 Hs.529846 Calcium modulating ligand CAMLG -1.40 5q23 Hs.193516 B-cell CLL/lymphoma 10 BCL10 -1.40 1p22 Hs.840 Indoleamine-pyrrole 2,3 dioxygenase INDO -1.40 8p12-p11 Hs.201083 Mal, T-cell differentiation protein 2 MAL2 -1.44 Hs.522805 CD99 antigen-like 2 CD99L2 -1.45 Xq28 Hs.50002 Chemokine (C-C motif) ligand 19 CCL19 -1.45 9p13 Hs.350268 Interferon regulatory factor 2 binding protein 2 IRF2BP2 -1.47 1q42.3 Hs.567249 Contactin 1 CNTN1 -1.47 12q11-q12 Hs.132807 MHC class I mRNA fragment 3.8-1 3.8-1 -1.48 6p21.3 Hs.416925 Carcinoembryonic antigen-related cell adhesion molecule 19 CEACAM19 -1.49 19q13.31 Hs.89546 Selectin E (endothelial -
Supplementary Materials
Journal of Alzheimer’s Disease 27 (2011) 1–9 1 IOS Press Supplementary Data Alzheimer’s Disease and Mild Cognitive Impairment are Associated with Elevated Levels of Isoaspartyl Residues in Blood Plasma Proteins Hongqian Yanga, Yaroslav Lyutvinskiya, Hilkka Soininenc and Roman A. Zubareva,b,∗ aDivision of Physiological Chemistry I, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden bScience for Life Laboratory, Stockholm, Sweden cDepartment of Neurology, School of Medicine, University of Eastern Finland, Kuopio, Finland Accepted 23 May 2011 SUPPLEMENTARY MATERIALS Supplementary Table S2 Subject age information for 96 individual samples Supplementary Table S1 Group No. of samples Age average Age std Age of the subjects for eight pooled blood plasma samples from 218 Control female 12 69 3.1 individuals: healthy Control. Control male 12 69 4.9 SMCI female 12 69 2.5 Group No. of subjects Age average Age std SMCI male 12 69 3.1 Control female 24 72 5.8 PMCI female 12 71 5.4 Control male 20 69 5.5 PMCI male 12 70 4.1 SMCI female 32 72 5.3 AD female 12 76 2.2 SMCI male 60 72 5.5 AD male 12 71 2.4 PMCI female 34 73 5.7 PMCI male 13 68 6.4 AD female 19 77 2.5 AD male 16 73 3.5 SMCI - stable mild cognitive impairment; PMCI - progressive mild cognitive impairment; AD - Alzheimer’s disease ∗Correspondence to: Roman A. Zubarev, E-mail: Roman. [email protected] ISSN 1387-2877/11/$27.50 © 2011 – IOS Press and the authors. -
Wo2017/132155
(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 2017/132155 Al 3 August 2017 (03.08.2017) P O P C T (51) International Patent Classification: (74) Agent: HUNTER-ENSOR, Melissa; c/o Greenberg A61K 45/00 (2006.01) C07K 16/18 (2006.01) Traurig LLP, One International Place, Boston, Massachu A61P 25/18 (2006.01) setts 021 10 (US). (21) International Application Number: (81) Designated States (unless otherwise indicated, for every PCT/US2017/014757 kind of national protection available): AE, AG, AL, AM, AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, (22) International Filing Date: BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DJ, DK, DM, 24 January 2017 (24.01 .2017) DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, (25) Filing Language: English HN, HR, HU, ID, IL, IN, IR, IS, JP, KE, KG, KH, KN, KP, KR, KW, KZ, LA, LC, LK, LR, LS, LU, LY, MA, (26) Publication Language: English MD, ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, (30) Priority Data: NI, NO, NZ, OM, PA, PE, PG, PH, PL, PT, QA, RO, RS, 62/286,867 25 January 2016 (25.01.2016) US RU, RW, SA, SC, SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, (71) Applicants: PRESIDENT AND FELLOWS OF HAR¬ ZA, ZM, ZW. VARD COLLEGE [US/US]; 17 Quincy Street, Cam bridge, Massachusetts 02138 (US).