DOCSLIB.ORG

TNFAIP3 / A20 Antibody Goat Polyclonal Antibody Catalog # ALS13001

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
TNFAIP3 / A20 Antibody Goat Polyclonal Antibody Catalog # ALS13001 10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 TNFAIP3 / A20 Antibody Goat Polyclonal Antibody Catalog # ALS13001 Specification TNFAIP3 / A20 Antibody - Product Information Application IHC Primary Accession P21580 Reactivity Human, Rabbit, Monkey Host Goat Clonality Polyclonal Calculated MW 90kDa KDa TNFAIP3 / A20 Antibody - Additional Information Gene ID 7128 Other Names Anti-TNFAIP3 antibody IHC of human small Tumor necrosis factor alpha-induced protein intestine. 3, TNF alpha-induced protein 3, 3.4.19.12, 6.3.2.-, OTU domain-containing protein 7C, Putative DNA-binding protein A20, Zinc TNFAIP3 / A20 Antibody - Background finger protein A20, A20p50, A20p37, TNFAIP3, OTUD7C Ubiquitin-editing enzyme that contains both ubiquitin ligase and deubiquitinase activities. Target/Specificity Involved in immune and inflammatory Human TNFAIP3. responses signaled by cytokines, such as TNF-alpha and IL-1 beta, or pathogens via Reconstitution & Storage Toll-like receptors (TLRs) through terminating Store at -20°C. Minimize freezing and NF-kappa-B activity. Essential component of a thawing. ubiquitin-editing protein complex, comprising also RNF11, ITCH and TAX1BP1, that ensures Precautions the transient nature of inflammatory signaling TNFAIP3 / A20 Antibody is for research use pathways. In cooperation with TAX1BP1 only and not for use in diagnostic or promotes disassembly of E2-E3 ubiquitin therapeutic procedures. protein ligase complexes in IL-1R and TNFR-1 pathways; affected are at least E3 ligases TRAF6, TRAF2 and BIRC2, and E2 TNFAIP3 / A20 Antibody - Protein Information ubiquitin-conjugating enzymes UBE2N and UBE2D3. In cooperation with TAX1BP1 Name TNFAIP3 promotes ubiquitination of UBE2N and proteasomal degradation of UBE2N and Synonyms OTUD7C UBE2D3. Upon TNF stimulation, deubiquitinates 'Lys-63'-polyubiquitin chains Function on RIPK1 and catalyzes the formation of Ubiquitin-editing enzyme that contains both 'Lys-48'-polyubiquitin chains. This leads to ubiquitin ligase and deubiquitinase RIPK1 proteasomal degradation and activities. Involved in immune and consequently termination of the TNF- or inflammatory responses signaled by LPS-mediated activation of NF-kappa-B. Page 1/3 10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 cytokines, such as TNF-alpha and IL-1 beta, Deubiquitinates TRAF6 probably acting on or pathogens via Toll-like receptors (TLRs) 'Lys-63'-linked polyubiquitin. Upon T-cell through terminating NF-kappa-B activity. receptor (TCR)-mediated T-cell activation, Essential component of a ubiquitin-editing deubiquitinates 'Lys-63'-polyubiquitin chains protein complex, comprising also RNF11, on MALT1 thereby mediating disassociation of ITCH and TAX1BP1, that ensures the the CBM (CARD11:BCL10:MALT1) and IKK transient nature of inflammatory signaling complexes and preventing sustained IKK pathways. In cooperation with TAX1BP1 activation. Deubiquitinates NEMO/IKBKG; the promotes disassembly of E2-E3 ubiquitin function is facilitated by TNIP1 and leads to protein ligase complexes in IL- 1R and inhibition of NF-kappa-B activation. Upon TNFR-1 pathways; affected are at least E3 stimulation by bacterial peptidoglycans, ligases TRAF6, TRAF2 and BIRC2, and E2 probably deubiquitinates RIPK2. Can also ubiquitin-conjugating enzymes UBE2N and inhibit I-kappa-B-kinase (IKK) through a UBE2D3. In cooperation with TAX1BP1 non-catalytic mechanism which involves promotes ubiquitination of UBE2N and proteasomal degradation of UBE2N and polyubiquitin; polyubiquitin promotes UBE2D3. Upon TNF stimulation, association with IKBKG and prevents IKK deubiquitinates 'Lys-63'-polyubiquitin MAP3K7-mediated phosphorylation. Targets chains on RIPK1 and catalyzes the TRAF2 for lysosomal degradation. In vitro able formation of 'Lys-48'-polyubiquitin chains. to deubiquitinate 'Lys-11'-, 'Lys-48'- and This leads to RIPK1 proteasomal 'Lys-63' polyubiquitin chains. Inhibitor of degradation and consequently termination programmed cell death. Has a role in the of the TNF- or LPS-mediated activation of function of the lymphoid system. Required for NF-kappa-B. Deubiquitinates TRAF6 LPS- induced production of proinflammatory probably acting on 'Lys-63'-linked cytokines and IFN beta in LPS-tolerized polyubiquitin. Upon T-cell receptor (TCR)- macrophages. mediated T-cell activation, deubiquitinates 'Lys-63'-polyubiquitin chains on MALT1 TNFAIP3 / A20 Antibody - References thereby mediating disassociation of the CBM (CARD11:BCL10:MALT1) and IKK Opipari A.W. Jr.,et al.J. Biol. Chem. complexes and preventing sustained IKK 265:14705-14708(1990). activation. Deubiquitinates NEMO/IKBKG; Ota T.,et al.Nat. Genet. 36:40-45(2004). the function is facilitated by TNIP1 and Mungall A.J.,et al.Nature 425:805-811(2003). leads to inhibition of NF-kappa-B activation. Mural R.J.,et al.Submitted (SEP-2005) to the Upon stimulation by bacterial EMBL/GenBank/DDBJ databases. peptidoglycans, probably deubiquitinates Bechtel S.,et al.BMC Genomics RIPK2. Can also inhibit I-kappa-B-kinase 8:399-399(2007). (IKK) through a non-catalytic mechanism which involves polyubiquitin; polyubiquitin promotes association with IKBKG and prevents IKK MAP3K7-mediated phosphorylation. Targets TRAF2 for lysosomal degradation. In vitro able to deubiquitinate 'Lys-11'-, 'Lys-48'- and 'Lys-63' polyubiquitin chains. Inhibitor of programmed cell death. Has a role in the function of the lymphoid system. Required for LPS-induced production of proinflammatory cytokines and IFN beta in LPS-tolerized macrophages. Cellular Location Cytoplasm. Nucleus. Lysosome. TNFAIP3 / A20 Antibody - Protocols Page 2/3 10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 Provided below are standard protocols that you may find useful for product applications. • Western Blot • Blocking Peptides • Dot Blot • Immunohistochemistry • Immunofluorescence • Immunoprecipitation • Flow Cytomety • Cell Culture Page 3/3 Powered by TCPDF (www.tcpdf.org).
Load more

Recommended publications
  • Laboratory Mouse Models for the Human Genome-Wide Associations
    Laboratory Mouse Models for the Human Genome-Wide Associations The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Kitsios, Georgios D., Navdeep Tangri, Peter J. Castaldi, and John P. A. Ioannidis. 2010. Laboratory mouse models for the human genome-wide associations. PLoS ONE 5(11): e13782. Published Version doi:10.1371/journal.pone.0013782 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:8592157 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA Laboratory Mouse Models for the Human Genome-Wide Associations Georgios D. Kitsios1,4, Navdeep Tangri1,6, Peter J. Castaldi1,2,4,5, John P. A. Ioannidis1,2,3,4,5,7,8* 1 Institute for Clinical Research and Health Policy Studies, Tufts Medical Center, Boston, Massachusetts, United States of America, 2 Tufts University School of Medicine, Boston, Massachusetts, United States of America, 3 Department of Hygiene and Epidemiology, University of Ioannina School of Medicine and Biomedical Research Institute, Foundation for Research and Technology-Hellas, Ioannina, Greece, 4 Tufts Clinical and Translational Science Institute, Tufts Medical Center, Boston, Massachusetts, United States of America, 5 Department of Medicine, Center for Genetic Epidemiology and Modeling, Tufts Medical Center, Tufts University
    [Show full text]
  • The UBE2L3 Ubiquitin Conjugating Enzyme: Interplay with Inflammasome Signalling and Bacterial Ubiquitin Ligases
    The UBE2L3 ubiquitin conjugating enzyme: interplay with inflammasome signalling and bacterial ubiquitin ligases Matthew James George Eldridge 2018 Imperial College London Department of Medicine Submitted to Imperial College London for the degree of Doctor of Philosophy 1 Abstract Inflammasome-controlled immune responses such as IL-1β release and pyroptosis play key roles in antimicrobial immunity and are heavily implicated in multiple hereditary autoimmune diseases. Despite extensive knowledge of the mechanisms regulating inflammasome activation, many downstream responses remain poorly understood or uncharacterised. The cysteine protease caspase-1 is the executor of inflammasome responses, therefore identifying and characterising its substrates is vital for better understanding of inflammasome-mediated effector mechanisms. Using unbiased proteomics, the Shenoy grouped identified the ubiquitin conjugating enzyme UBE2L3 as a target of caspase-1. In this work, I have confirmed UBE2L3 as an indirect target of caspase-1 and characterised its role in inflammasomes-mediated immune responses. I show that UBE2L3 functions in the negative regulation of cellular pro-IL-1 via the ubiquitin- proteasome system. Following inflammatory stimuli, UBE2L3 assists in the ubiquitylation and degradation of newly produced pro-IL-1. However, in response to caspase-1 activation, UBE2L3 is itself targeted for degradation by the proteasome in a caspase-1-dependent manner, thereby liberating an additional pool of IL-1 which may be processed and released. UBE2L3 therefore acts a molecular rheostat, conferring caspase-1 an additional level of control over this potent cytokine, ensuring that it is efficiently secreted only in appropriate circumstances. These findings on UBE2L3 have implications for IL-1- driven pathology in hereditary fever syndromes, and autoinflammatory conditions associated with UBE2L3 polymorphisms.
    [Show full text]
  • Efficient Analysis of Mouse Genome Sequences Reveal Many Nonsense Variants
    Efficient analysis of mouse genome sequences reveal many nonsense variants Sophie Steelanda,b,1, Steven Timmermansa,b,1, Sara Van Ryckeghema,b, Paco Hulpiaua,b, Yvan Saeysa,c, Marc Van Montagud,e,f,2, Roosmarijn E. Vandenbrouckea,b,3, and Claude Liberta,b,2,3 aInflammation Research Center, Flanders Institute for Biotechnology (VIB), 9052 Ghent, Belgium; bDepartment of Biomedical Molecular Biology, Ghent University, 9052 Ghent, Belgium; cDepartment of Internal Medicine, Ghent University, 9052 Ghent, Belgium; dDepartment of Plant Systems Biology, VIB, 9052 Ghent, Belgium; eDepartment of Plant Biotechnology and Bioinformatics, Ghent University, 9052 Ghent, Belgium; and fInternational Plant Biotechnology Outreach, VIB, Ghent, Belgium Contributed by Marc Van Montagu, March 30, 2016 (sent for review December 31, 2015; reviewed by Bruce Beutler, Stefano Bruscoli, Stefan Rose-John, and Klaus Schulze-Osthoff) Genetic polymorphisms in coding genes play an important role alive, archiving them, and distributing mutant strains to in- when using mouse inbred strains as research models. They have terested users (4). been shown to influence research results, explain phenotypical Since Clarence Little showed in the early 20th century that the differences between inbred strains, and increase the amount of principle of inbreeding also applies to mice, several hundred interesting gene variants present in the many available inbred inbred mouse strains have been generated (5). Some of these lines. SPRET/Ei is an inbred strain derived from Mus spretus that strains display specific phenotypes that are the result of a mutant has ∼1% sequence difference with the C57BL/6J reference ge- gene, and in several cases have formed the basis for identifying nome.
    [Show full text]
  • Targeting Lymphomas Through MALT1 Inhibition
    www.impactjournals.com/oncotarget/ Oncotarget, December, Vol.3, No 12 Targeting Lymphomas Through MALT1 Inhibition Lorena Fontan and Ari Melnick Diffuse large B-cell lymphoma (DLBCL), the most contain mutations in TLR and BCR signaling components common form of non-Hodgkin Lymphoma, comprises [4, 5]. These data revealed that MALT1 is a bona fide a heterogeneous group of diseases that can be classified therapeutic target, inhibition of which may disrupt into at least three different entities with distinct gene oncogenic signaling induced by somatic mutations in expression signatures. Among these, the activated B ABC-DLBCLs. However Z-VRPR-FMK is not suitable cell-like (ABC)-DLBCLs are the most resistant to as a therapeutic agent due its unfavorable pharmacological current standard immune-chemotherapy regimens [1]. properties. Development of novel targeted therapies with activity Fortunately, two recent studies identified small in this DLBCL subtype is required to improve clinical molecule inhibitors of the MALT1 protease activity outcome for these patients. with potent activity against ABC-DLBCL cells both Efforts to identify recurrent somatic mutations in in vitro and in vivo [6, 7]. One of the studies identified ABC-DLBCLs have revealed common biological themes phenothiazine compounds as mediating reversible MALT1 despite their considerable genetic heterogeneity. Most cleavage inhibition [7]; whereas the other identified a notably frequent activating somatic mutation in B-cell novel compound termed “MALT1 inhibitor-2” (MI- receptor (BCR) and Toll like receptor (TLR) signaling 2), that irreversibly binds the active site of MALT1 and pathways, leading to constitutive NF-κB activity [2]. potently suppresses its enzymatic activity at nanomolar Along these lines the MALT1 paracaspase has emerged as concentrations [6].
    [Show full text]
  • Ufmylation Inhibits the Proinflammatory Capacity of Interferon-Γ–Activated Macrophages
    UFMylation inhibits the proinflammatory capacity of interferon-γ–activated macrophages Dale R. Balcea,1,2, Ya-Ting Wanga,b, Michael R. McAllasterb,1, Bria F. Dunlapa, Anthony Orvedahlc, Barry L. Hykes Jra, Lindsay Droita, Scott A. Handleya, Craig B. Wilend,e, John G. Doenchf, Robert C. Orchardg, Christina L. Stallingsb, and Herbert W. Virgina,1,2 aDepartment of Pathology and Immunology, Washington University School of Medicine in St. Louis, St. Louis, MO 63110; bDepartment of Molecular Microbiology, Washington University School of Medicine in St. Louis, St. Louis, MO 63110; cDepartment of Pediatrics, Washington University School of Medicine in St. Louis, St. Louis, MO 63110; dDepartment of Laboratory Medicine, Yale School of Medicine, New Haven, CT 06510; eDepartment of Immunobiology, Yale School of Medicine, New Haven, CT 06510; fBroad Institute of MIT and Harvard, Cambridge, MA 02142; and gDepartment of Immunology and Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75390 Contributed by Herbert W. Virgin, November 19, 2020 (sent for review June 15, 2020; reviewed by Masaaki Komatsu and Hong Zhang) Macrophages activated with interferon-γ (IFN-γ) in combination in regulating this aspect of cellular immunity. Thus, understanding with other proinflammatory stimuli, such as lipopolysaccharide pathways that positively and negatively regulate IFN-γ–dependent or tumor necrosis factor-α (TNF-α), respond with transcriptional macrophage activation is an important priority. and cellular changes that enhance clearance of intracellular path- Here we performed a genome-wide CRISPR screen to identify ogens at the risk of damaging tissues. IFN-γ effects must therefore proteins that negatively regulate IFN-γ responses in macrophages.
    [Show full text]
  • Association of TNFAIP3 Polymorphism with Rheumatic Heart Disease in Chinese Han Population
    Immunogenetics (2009) 61:739–744 DOI 10.1007/s00251-009-0405-8 ORIGINAL PAPER Association of TNFAIP3 polymorphism with rheumatic heart disease in Chinese Han population Rong Hua & Ji-bin Xu & Jiu-cun Wang & Li Zhu & bing Li & Yang Liu & Sheng-dong Huang & Li Jin & Zhi-yun Xu & Xiao-feng Wang Received: 6 September 2009 /Accepted: 13 October 2009 /Published online: 10 November 2009 # Springer-Verlag 2009 Abstract In a pair-matched case–control study (239 versus (p=0.000). Under a dominant model, CC/CT carriers had 478) conducted in Chinese Han population, we investigated a 0.54-fold reduced risk of RHD (95% confidence interval the association between tumor necrosis factor-α-induced 0.38–0.75, p=0.000) than TT carriers. Therefore, we report protein 3 (TNFAIP3) gene, tumor necrosis factor receptor- a new genetic variant (rs582757) in the TNFAIP3 gene that associated factor 1 (TRAF1) gene, complement component associated with the prevalence of RHD in Chinese Han 5 (C5) gene, and rheumatic heart disease (RHD). We population. Further genetic and functional studies are observed no association with RHD for the five tagging required to identify the etiological variants in linkage single nucleotide polymorphisms (tSNP) in the C5 gene, disequilibrium with this polymorphism. the three tSNPs in the TNFAIP3 gene, or the two tSNPs in the TRAF1 gene. However, we determined that the tSNP, Keywords Rheumatic heart disease . Polymorphism . rs582757, located at intron_5 of the TNFAIP3 gene, Genetics . Association associated with RHD in Chinese Han population. Both the distribution of genotype and allele frequencies differed significantly between case and control subjects (p=0.001 Introduction and p=0.0004, respectively).
    [Show full text]
  • The Human Gene Connectome As a Map of Short Cuts for Morbid Allele Discovery
    The human gene connectome as a map of short cuts for morbid allele discovery Yuval Itana,1, Shen-Ying Zhanga,b, Guillaume Vogta,b, Avinash Abhyankara, Melina Hermana, Patrick Nitschkec, Dror Friedd, Lluis Quintana-Murcie, Laurent Abela,b, and Jean-Laurent Casanovaa,b,f aSt. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065; bLaboratory of Human Genetics of Infectious Diseases, Necker Branch, Paris Descartes University, Institut National de la Santé et de la Recherche Médicale U980, Necker Medical School, 75015 Paris, France; cPlateforme Bioinformatique, Université Paris Descartes, 75116 Paris, France; dDepartment of Computer Science, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel; eUnit of Human Evolutionary Genetics, Centre National de la Recherche Scientifique, Unité de Recherche Associée 3012, Institut Pasteur, F-75015 Paris, France; and fPediatric Immunology-Hematology Unit, Necker Hospital for Sick Children, 75015 Paris, France Edited* by Bruce Beutler, University of Texas Southwestern Medical Center, Dallas, TX, and approved February 15, 2013 (received for review October 19, 2012) High-throughput genomic data reveal thousands of gene variants to detect a single mutated gene, with the other polymorphic genes per patient, and it is often difficult to determine which of these being of less interest. This goes some way to explaining why, variants underlies disease in a given individual. However, at the despite the abundance of NGS data, the discovery of disease- population level, there may be some degree of phenotypic homo- causing alleles from such data remains somewhat limited. geneity, with alterations of specific physiological pathways under- We developed the human gene connectome (HGC) to over- come this problem.
    [Show full text]
  • Haploinsufficiency of A20 Impairs Protein–Protein Interactome and Leads Into Caspase-8-Dependent Enhancement of NLRP3 Inflammasome Activation
    Autoinflammatory disorders RMD Open: first published as 10.1136/rmdopen-2018-000740 on 17 October 2018. Downloaded from ORIGINAL ARTICLE Haploinsufficiency of A20 impairs protein–protein interactome and leads into caspase-8-dependent enhancement of NLRP3 inflammasome activation Kristiina Rajamäki,1 Salla Keskitalo,2 Mikko Seppänen,3 Outi Kuismin,4 Paula Vähäsalo,5 Luca Trotta,6 Antti Väänänen,7 Virpi Glumoff,8 Paula Keskitalo,5 Riitta Kaarteenaho,9,10 Airi Jartti,11 Nina Hautala,12 Päivi Jackson,12 Dan C Nordström,13 Janna Saarela,6 Timo Hautala,14 Kari K Eklund,15,16,17 Markku Varjosalo2,18 To cite: Rajamäki K, ABSTRACT Key messages Keskitalo S, Seppänen M, Objectives TNFAIP3 encodes A20 that negatively et al. Haploinsufficiency regulates nuclear factor kappa light chain enhancer of of A20 impairs protein– What is already known about this subject? activated B cells (NF-κB), the major transcription factor protein interactome and A20 is a negative regulator of nuclear factor kappa B coordinating inflammatory gene expression.TNFAIP3 ► leads into caspase-8- (NF- B) having a key role in immune activation and polymorphisms have been linked with a spectrum of κ dependent enhancement autoimmunity. inflammatory and autoimmune diseases and, recently, of NLRP3 inflammasome Loss-of-function mutations in A20 are reported to loss-of-function mutations in A20 were found to cause ► activation. RMD Open lead to an inflammatory disease termed haploinsuf- 2018;4:e000740. doi:10.1136/ a novel inflammatory disease ‘haploinsufficiency ofA 20’ ficiency ofA 20 (HA20). rmdopen-2018-000740 (HA20). Here we describe a family with HA20 caused by a novel TNFAIP3 loss-of-function mutation and elucidate What does this study add? ► Prepublication history and the upstream molecular mechanisms linking HA20 to ► We report a novel p.(Lys91*) A20 mutation and use it additional material for this dysregulation of NF-κB and the related inflammasome as a model to uncover molecular mechanisms relat- paper are available online.
    [Show full text]
  • Construction and Analysis of Protein-Protein Interaction Network of Non-Alcoholic Fatty Liver Disease
    bioRxiv preprint doi: https://doi.org/10.1101/2020.12.01.406215; this version posted December 9, 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. Construction and Analysis of Protein-Protein Interaction Network of Non-Alcoholic Fatty Liver Disease Athina I. Amanatidou and George V. Dedoussis Department of Nutrition and Dietetics, School of Health Science and Education, Harokopio University, El. Venizelou 70, 17671, Athens, Greece Correspondence to: G. V. Dedoussis, A. I. Amanatidou, Department of Nutrition and Dietetics, School of Health Science and Education, Harokopio University, El. Venizelou 70, 17671, Athens, Greece E-mail addresses: [email protected] (G.V. Dedoussis), [email protected] (A. I. Amanatidou) Telephone: +302109549179 (G.V. Dedoussis), +306949293472 (A. I. Amanatidou) 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.12.01.406215; this version posted December 9, 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 Non-alcoholic fatty liver disease (NAFLD) is a disease with multidimensional complexities. Many attempts have been made over the years to treat this disease but its incidence is rising. For this reason, the need to identify and study new candidate proteins that may be associated with NAFLD is of utmost importance. Systems-based approaches such as the analysis of protein-protein interaction (PPI) network could lead to the discovery of new proteins associated with a disease that can then be translated into clinical practice.
    [Show full text]
  • Original Article TNFAIP3 Rs2230926 Polymorphisms in Rheumatoid Arthritis of Southern Chinese Han Population: a Case-Control Study
    Int J Clin Exp Pathol 2014;7(12):8958-8961 www.ijcep.com /ISSN:1936-2625/IJCEP0003268 Original Article TNFAIP3 rs2230926 polymorphisms in rheumatoid arthritis of southern Chinese Han population: a case-control study Guifeng Hao1, Yasong Li1, Jinlin Liu2, Mingyi Wo2 1Department of Rheumatology, Zhejiang Provencial People’s Hospital, Hangzhou 310014, Zhejiang, China; 2Department of Clinical Laboratory, Zhejiang Provencial People’s Hospital, Hangzhou 310014, Zhejiang, China Received October 20, 2014; Accepted December 1, 2014; Epub December 1, 2014; Published December 15, 2014 Abstract: Polymorphism of tumor necrosis factor alpha-induced protein 3 (TNFAIP3) has been be related to various auto-immune diseases. Based on previous studies that the single nucleotide polymorphism (SNP) of rs2230926 was association with rheumatoid arthritis (RA) of Japanese, Caucasian population and the northern Chinese Han population, we tested the alleles and geno-type frequencies of rs2230926 in TNFAIP3 to investigate whether rs2230926 is susceptible to RA of southern Chinese Han population. In our case-control association study, 207 RA patients fulfilling the American College of Rheumatology (ACR)1987 criteria were compared with 199 unrelated healthy subjects. After testing the alleles and genotype frequencies of rs2230926, the airwise linkage disequi- librium (LD) was computed and odd ration (OR) and 95% confidence intervals (95% CI) were used for evaluating the susceptibility to RA. The SNP of rs2230926 of the cases and control subjects were conformed to the Hardy- Weinberg equilibrium (P = 0.02257). The significantly statistical differences in alleles of T, G were founded in the cases and controls (P = 0.0027, OR 0.417, 95% CI 0.232-0.749); the genetic types of rs2230926 were associated with a susceptibility to RA, with OR 0.375 (95% CI 0.198-0.707, P = 0.0018).
    [Show full text]
  • Rabbit Anti-IKK Gamma/FITC Conjugated Antibody-SL2898R-FITC
    SunLong Biotech Co.,LTD Tel: 0086-571- 56623320 Fax:0086-571- 56623318 E-mail:[email protected] www.sunlongbiotech.com Rabbit Anti-IKK gamma/FITC Conjugated antibody SL2898R-FITC Product Name: Anti-IKK gamma/FITC Chinese Name: FITC标记的KB抑制蛋白激酶γ抗体 IkB kinase associated protein 1; IkB kinase subunit gamma; Inhibitor of nuclear factor kappa B kinase subunit gamma; AMCBX1; FIP 3; FIP3; Fip3p; I kappa B kinase gamma; IkB kinase associated protein 1; IkB kinase gamma subunit; IkB kinase subunit gamma; IKBKG; IKKAP 1; IKKAP1; IKKG; Incontinentia pigmenti; Inhibitor of kappa light polypeptide gene enhancer in B cells kinase gamma; Inhibitor of kappa light Alias: polypeptide gene enhancer in B cells, kinase gamma; Inhibitor of nuclear factor kappa B kinase gamma subunit; Inhibitor of nuclear factor kappa B kinase subunit gamma; IP 1; IP 2; IP; IP1; IP2; IPD2; NEMO; NF kappa B essential modifier; NF kappa B essential modulator; NF kappaB essential modifier; NF kappaB essential modulator; NFkappaB essential modulator. Organism Species: Rabbit Clonality: Polyclonal React Species: Human,Mouse,Rat,Dog,Pig,Horse,Rabbit, IF=1:50-200 Applications: not yet tested in other applications. optimalwww.sunlongbiotech.com dilutions/concentrations should be determined by the end user. Molecular weight: 46kDa Form: Lyophilized or Liquid Concentration: 1mg/ml immunogen: KLH conjugated synthetic peptide derived from human IKK gamma Lsotype: IgG Purification: affinity purified by Protein A Storage Buffer: 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year Storage: when kept at -20°C.
    [Show full text]
  • Molecular Insights Into the Pathogenesis of Follicular Lymphoma
    13 Review Article Page 1 of 13 Molecular insights into the pathogenesis of follicular lymphoma Ting Zhou, Stefania Pittaluga, Elaine S. Jaffe Hematopathology Section, Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA Contributions: (I) Conception and design: All authors; (II) Administrative support: None; (III) Provision of study materials or patients: None; (IV) Collection and assembly of data: None; (V) Data analysis and interpretation: None; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors. Correspondence to: Dr. Elaine S. Jaffe. 10 Center Drive, Room 3S 235, National Institutes of Health, Bethesda, MD 20892, USA. Email: [email protected]. Abstract: Follicular lymphoma (FL) represents a group of B-cell neoplasms derived from germinal center (GC) B cells. A better understanding of the pathogenic mechanisms of FL is important for developing innovative therapies. The most common form of FL is primarily nodal and associated with the t(14;18). Recent advances obtained via genomic profiling have provided unprecedented insights into the pathogenesis of FL. Conventional FL evolves through multiple independent or convergent genetic pathways. The classical pathogenesis of t(14;18)-positive FL is a multi-stage and multi-hit process escalating along accumulation of genetic and epigenetic alterations, which starts from FL-like B cells, through premalignant lesions, into full-blown malignancy. Early precursor lesions have been recognized in the form of FL-like B cells in normal peripheral blood, and both in-situ follicular neoplasia (ISFN) and duodenal-type FL. In comparison, t(14;18)-negative FL is much more heterogeneous at the molecular level, and the underlying mechanisms are less well understood.
    [Show full text]