Complement Component 4B (C4b) Organism: Mus Musculus (Mouse) Instruction Manual

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P91305Mu01 Complement Component 4b (C4b) Organism: Mus musculus (Mouse) Instruction manual FOR IN VITRO USE AND RESEARCH USE ONLY NOT FOR USE IN DIAGNOSTIC OR THERAPEUTIC PROCEDURES 3th Edition (Revised in February, 2012) [ DESCRIPTION ] Protein Names: Complement Component 4b Gene Names: C4b Size: 100µg Source: Recombinant Expression Host: E.coli Function: C4 plays a central role in the activation of the classical pathway of the complement system. It is processed by activated C1 which removes from the alpha chain the C4a anaphylatoxin. The remaining alpha chain fragment C4b is the major activation product and is an essential subunit of the C3 convertase (C4b2a) and the C5 convertase (C3bC4b2a) enzymes of the classical complement pathway. Subcellular Location: Secreted [ PROPERTIES ] Residues: Asn678-Arg753 (Accession # P01029), with a N-terminal His-tag. Grade & Purity: >97%, 10.24 kDa as determined by SDS-PAGE reducing conditions. Form & Buffer: Supplied as lyophilized form in PBS, pH 7.4. Endotoxin Level: <1.0 EU per 1μg (determined by the LAL method). Applications: SDS-PAGE; WB; ELISA; IP. (May be suitable for use in other assays to be determined by the end user.) Predicted Molecular Mass: 10.24 kDa [ PREPARATION ] Reconstitute in PBS. [ STORAGE AND STABILITY ] Storage: Store at 4oC for short time storage (1-2 weeks). Aliquot and store at -20oC or -80oC for long term storage. Avoid repeated freeze/thaw cycles. Valid period: 12 months stored at -80oC. [ BACKGROUND] The target protein is fused with a His-tag and its sequence is listed below. The first Met is an initiator amino acid. Moreover, Gly and Ser are added to improve the flexibility of N-terminus at both ends of the His-tag, which will increase the chelating ability of the tag to Ni-Sepharose during purification. MGHHHHHHSGSEF-NVN FQKAVSEKLG QYSSPDAKRC CQDGMTKLPM KRTCEQRAAR VPQQACREPF LSCCKFAEDL RRNQTRSQAH LAR [ REFERENCES ] 1. Ogata R.T., et al. (1989) J. Biol. Chem. 264:16565-16572. 2. Nonaka M., et al. (1985) Immunol. Rev. 87:81-99..

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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.
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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.
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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).
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Supporting Information for Proteomics DOI 10.1002/Prca.200780101
Supporting Information for Proteomics DOI 10.1002/prca.200780101 Paul Cutler, Emma L. Akuffo, Wanda M. Bodnar, Deborah M. Briggs, John B. Davis, Christine M. Debouck, Steven M. Fox, Rachel A. Gibson, Darren A. Gormley, Joanna D. Holbrook, A. Jacqueline Hunter, Emma E. Kinsey, Rabinder Prinjha, Jill C. Richardson, Allen D. Roses, Marjorie A. Smith, Nikos Tsokanas, David R. Will, Wen Wu, John W. Yates and Israel S. Gloger Proteomic identification and early validation of complement 1 inhibitor and pigment epithelium-derived factor: Two novel biomarkers of Alzheimer’s disease in human plasma ª 2007 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.clinical.proteomics-journal.com Supplementary Table 1: Complete list of proteins identified from spots derived from 2D gel analysis of human plasma. Each protein was observed to be in a spot showing altered expression between Alzheimer’s disease and matched control by statistical methods as described in the Methods section. Each protein is identified by the gene description and the HUGO gene symbol. The number of “changing” spots in which this protein was observed is also given. HUGO Human Gene Number of Gene Description Symbol Spots alpha-1-B glycoprotein; A1BG 5 alpha-2-macroglobulin A2M 7 afamin; AFM 1 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) AGT 4 alpha-2-HS-glycoprotein AHSG 3 albumin ALB 90 alpha-1-microglobulin/bikunin precursor; AMBP 1 annexin A1 ANXA1 1 amyloid P component, serum APCS 3 apolipoprotein A-I APOA1 14 apolipoprotein A-IV APOA4 2 apolipoprotein E APOE 2 apolipoprotein
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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.
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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).
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Rabbit Anti-Complement C4 Gamma Chain/FITC Conjugated Antibody
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Table S5.6 HEPG2 Co-Culture Vs Worm-Free Down-Regulated Genes
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Complement System in the Pathogenesis of Benign Lymphoepithelial Lesions of the Lacrimal Gland
RESEARCH ARTICLE Complement System in the Pathogenesis of Benign Lymphoepithelial Lesions of the Lacrimal Gland Jing Li1,2, Xin Ge1, Xiaona Wang1,2, Xiao Liu1, Jianmin Ma1* 1 Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing, China, 2 Beijing Institute of Ophthalmology, Beijing Tongren Hospital, Capital Medical University, Beijing, China * [email protected] Abstract Objective We aimed to examine the potential involvement of local complement system gene expres- sion in the pathogenesis of benign lymphoepithelial lesions (BLEL) of the lacrimal gland. OPEN ACCESS Citation: Li J, Ge X, Wang X, Liu X, Ma J (2016) Methods Complement System in the Pathogenesis of Benign We collected data from 9 consecutive pathologically confirmed patients with BLEL of the Lymphoepithelial Lesions of the Lacrimal Gland. PLoS ONE 11(2): e0148290. doi:10.1371/journal. lacrimal gland and 9 cases with orbital cavernous hemangioma as a control group, and pone.0148290 adopted whole genome microarray to screen complement system-related differential Editor: Qiang WANG, Sichuan University, CHINA genes, followed by RT-PCR verification and in-depth enrichment analysis (Gene Ontology analysis) of the gene sets. Received: September 26, 2015 Accepted: January 15, 2016 Results Published: February 5, 2016 The expression of 14 complement system-related genes in the pathologic tissue, including Copyright: © 2016 Li et al. This is an open access C2, C3, ITGB2, CR2, C1QB, CR1, ITGAX, CFP, C1QA, C4B|C4A, FANCA, C1QC, C3AR1 article distributed under the terms of the Creative and CFHR4, were significantly upregulated while 7 other complement system-related Commons Attribution License, which permits genes, C5, CFI, CFHR1|CFH, CFH, CD55, CR1L and CFD were significantly downregulated unrestricted use, distribution, and reproduction in any medium, provided the original author and source are in the lacrimal glands of BLEL patients.
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Anti-C4B Monoclonal Antibody, Clone FQS21254 (DCABH-5518) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use
Anti-C4B monoclonal antibody, clone FQS21254 (DCABH-5518) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Product Overview Rabbit monoclonal to C4a Antigen Description C4 plays a central role in the activation of the classical pathway of the complement system. It is processed by activated C1 which removes from the alpha chain the C4a anaphylatoxin. The remaining alpha chain fragment C4b is the major activation product and is an essential subunit of the C3 convertase (C4b2a) and the C5 convertase (C3bC4b2a) enzymes of the classical complement pathway.Derived from proteolytic degradation of complement C4, C4a anaphylatoxin is a mediator of local inflammatory process. It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes. Immunogen Recombinant fragment within Human C4a. The exact sequence is proprietary.Database link: P0C0L4 Isotype IgG Source/Host Rabbit Species Reactivity Human Clone FQS21254 Purity Tissue culture supernatant Conjugate Unconjugated Applications Flow Cyt, IHC-P, WB Positive Control HepG2 cell lysate; Human colon and stomach tissues; HepG2 cells. Format Liquid Size 100 μl Buffer Preservative: 0.01% Sodium azide; Constituents: 50% Glycerol, 0.05% BSA Preservative 0.01% Sodium Azide Storage Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle. 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel:
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