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CCR7 Antibody (Y59) NB110-55680
Product Datasheet CCR7 Antibody (Y59) NB110-55680 Unit Size: 0.1 ml Store at -20C. Avoid freeze-thaw cycles. Publications: 9 Protocols, Publications, Related Products, Reviews, Research Tools and Images at: www.novusbio.com/NB110-55680 Updated 5/28/2019 v.20.1 Earn rewards for product reviews and publications. Submit a publication at www.novusbio.com/publications Submit a review at www.novusbio.com/reviews/destination/NB110-55680 Page 1 of 6 v.20.1 Updated 5/28/2019 NB110-55680 CCR7 Antibody (Y59) Product Information Unit Size 0.1 ml Concentration This product is unpurified. The exact concentration of antibody is not quantifiable. Storage Store at -20C. Avoid freeze-thaw cycles. Clonality Monoclonal Clone Y59 Preservative 0.01% Sodium Azide Isotype IgG Purity Tissue culture supernatant Buffer 49% PBS, 0.05% BSA and 50% Glycerol Target Molecular Weight 45 kDa Product Description Host Rabbit Gene ID 1236 Gene Symbol CCR7 Species Human, Mouse, Rat, Monkey Reactivity Notes May cross reacts with Rhesus monkey. Specificity/Sensitivity The antibody does not cross-react with other G-protein coupled receptor 1 family members. Immunogen A synthetic peptide corresponding to residues in N-terminal extracellular domain of human CKR7 was used as immunogen. Notes Produced using Abcam's RabMab® technology. RabMab® technology is covered by the following U.S. Patents, No. 5,675,063 and/or 7,429,487. Product Application Details Applications Western Blot, Immunocytochemistry/Immunofluorescence, Immunohistochemistry, Immunohistochemistry-Frozen, Immunohistochemistry- Paraffin, Immunoprecipitation, Flow Cytometry (Negative) Recommended Dilutions Western Blot 1:1000-10000, Immunohistochemistry 1:10-1:500, Immunocytochemistry/Immunofluorescence 1:250, Immunoprecipitation 1:10, Immunohistochemistry-Paraffin 1:250, Immunohistochemistry-Frozen 1:250, Flow Cytometry (Negative) Application Notes This product is useful for: Western Blot, Immunohistochemistry-Paraffin, Immunocytochemistry, Immunoprecipitation. -
Chemokine Receptors in Allergic Diseases Laure Castan, A
Chemokine receptors in allergic diseases Laure Castan, A. Magnan, Grégory Bouchaud To cite this version: Laure Castan, A. Magnan, Grégory Bouchaud. Chemokine receptors in allergic diseases. Allergy, Wiley, 2017, 72 (5), pp.682-690. 10.1111/all.13089. hal-01602523 HAL Id: hal-01602523 https://hal.archives-ouvertes.fr/hal-01602523 Submitted on 11 Jul 2018 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Distributed under a Creative Commons Attribution - ShareAlike| 4.0 International License Allergy REVIEW ARTICLE Chemokine receptors in allergic diseases L. Castan1,2,3,4, A. Magnan2,3,5 & G. Bouchaud1 1INRA, UR1268 BIA; 2INSERM, UMR1087, lnstitut du thorax; 3CNRS, UMR6291; 4Universite de Nantes; 5CHU de Nantes, Service de Pneumologie, Institut du thorax, Nantes, France To cite this article: Castan L, Magnan A, Bouchaud G. Chemokine receptors in allergic diseases. Allergy 2017; 72: 682–690. Keywords Abstract asthma; atopic dermatitis; chemokine; Under homeostatic conditions, as well as in various diseases, leukocyte migration chemokine receptor; food allergy. is a crucial issue for the immune system that is mainly organized through the acti- Correspondence vation of bone marrow-derived cells in various tissues. Immune cell trafficking is Gregory Bouchaud, INRA, UR1268 BIA, rue orchestrated by a family of small proteins called chemokines. -
Memoranaurns by the Participants in Signes Par Les Partici- I the Meeting
Memoranda are state- Les Memorandums ments concerning the exposent les conclu- /e , conclusions or recom- sions et recomman- M e mmooranrantedaa mendations of certain dations de certaines / a t w / /WHO scientific meet- /reunions scientifiques ings; they are signed de /'OMS; ils sont Memoranaurns by the participants in signes par les partici- I the meeting. pants a ces reunions. Bulletin ofthe World Health Organization, 62 (2): 217-227 (1984) © World Health Organization 1984 Immunodiagnosis simplified: Memorandum from a WHO Meeting* Technologies suitable for the development ofsimplified immunodiagnostic tests were reviewed by a Working Group of the WHO Advisory Committee on Medical Research in Geneva in June 1983. They included agglutination tests and use ofartificialparticles coated with immunoglobulins, direct visual detection of antigen-antibody reactions, enzyme- immunoassays, and immunofluorescence and fluoroimmunoassays. The use of mono- clonal antibodies,in immunodiagnosis and of DNA /RNA probes to identify viruses was also discussed in detail. The needfor applicability of these tests at three levels, i.e., field conditions (or primary health care level), local laboratories, and central laboratories, was discussed and their use at thefield level was emphasized. Classical serological techniques have been used for All these tests can be carried out in laboratories that a long time for diagnostic purposes, e.g., for con- are equipped with basic instruments as well as special- firmation of clinical diagnoses, epidemiological ized apparatus (e.g., gamma counters for RIA, ultra- studies, testing of blood donors, etc. Some of these violet microscopes for IMF, etc.), which are usually techniques have been standardized to a high degree of available only in the larger, central laboratories. -
Cytokine Immunocytochemistry Fax (65) 860-1590 Fax (49) 40 531 58 92 Fax (81) 3 541-381-55 E-Mail: [email protected]
PharMingen International United States Canada PharMingen Europe Japan PharMingen Canada Tel 619-812-8800 Asia Pacific Becton Dickinson GmbH Nippon Becton Dickinson Toll-Free 1-888-259-0187 Orders 1-800-848-6227 BD Singapore HQ PharMingen Europe Company Ltd. Tel 905-542-8028 Tech Service 1-800-825-5832 Tel (65) 860-1478 Tel (49) 40 532 84 48 0 Tel (81) 3 541-382-51 Fax 905-542-9391 Fax 619-812-8888 Cytokine Immunocytochemistry Fax (65) 860-1590 Fax (49) 40 531 58 92 Fax (81) 3 541-381-55 e-mail: [email protected] http://www.pharmingen.com Africa Germany Latin/South America Spain Becton Dickinson Worldwide Inc. Becton Dickinson GmbH BDIS (USA) Becton Dickinson S.A. Reagents and Techniques Tel (254) 2 449 608 HQ PharMingen Europe Tel (408) 954-2157 Tel (34) 91 848 8100 Fax (254) 2 449 619 Tel (49) 40 532 84 48 0 Fax (408) 526-1804 Fax (34) 91 848 8105 Fax (49) 40 531 58 92 Orders for Microscopic Analysis of Cytokine-Producing Cells Australia Malaysia Tel (34) 91 848 8182 Becton Dickinson Pty Ltd Greece Becton Dickinson Sdn Bhd Fax (34) 91 848 8104 Tel (612) 9978-6800 Becton Dickinson Hellas S.A. Tel (03) 7571323 Fax (612) 9978-6850 Tel (30) 1 9407741 Fax (03) 7571153 Sweden Fax (30) 1 9407740 Becton Dickinson AB Austria Mexico Tel (46) 8 775 51 00 Becton Dickinson GmbH Hong Kong Becton Dickinson de Mexico Fax (46) 8 645 08 08 HQ PharMingen Europe Becton Dickinson Asia Ltd Tel (52-5) 237-12-98 Tel (49) 40 532 84 48 0 Tel (852) 2572-8668 Fax (52-5) 237-12-93 Switzerland Fax (49) 40 531 58 92 Fax (852) 2520-1837 Becton Dickinson GmbH Middle East HQ PharMingen Europe Belgium Hungary Becton Dickinson Tel (41) 06 1-385 4422 Becton Dickinson Benelux N.V. -
Mice in Inflammation Psoriasiform Skin IL-22 Is Required for Imiquimod-Induced
IL-22 Is Required for Imiquimod-Induced Psoriasiform Skin Inflammation in Mice Astrid B. Van Belle, Magali de Heusch, Muriel M. Lemaire, Emilie Hendrickx, Guy Warnier, Kyri This information is current as Dunussi-Joannopoulos, Lynette A. Fouser, Jean-Christophe of September 29, 2021. Renauld and Laure Dumoutier J Immunol published online 30 November 2011 http://www.jimmunol.org/content/early/2011/11/30/jimmun ol.1102224 Downloaded from Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on September 29, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2011 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published November 30, 2011, doi:10.4049/jimmunol.1102224 The Journal of Immunology IL-22 Is Required for Imiquimod-Induced Psoriasiform Skin Inflammation in Mice Astrid B. Van Belle,*,† Magali de Heusch,*,† Muriel M. Lemaire,*,† Emilie Hendrickx,*,† Guy Warnier,*,† Kyri Dunussi-Joannopoulos,‡ Lynette A. Fouser,‡ Jean-Christophe Renauld,*,†,1 and Laure Dumoutier*,†,1 Psoriasis is a common chronic autoimmune skin disease of unknown cause that involves dysregulated interplay between immune cells and keratinocytes. -
Metamorphic Protein Folding Encodes Multiple Anti-Candida Mechanisms in XCL1
pathogens Article Metamorphic Protein Folding Encodes Multiple Anti-Candida Mechanisms in XCL1 Acacia F. Dishman 1,2,†, Jie He 3,†, Brian F. Volkman 1,* and Anna R. Huppler 3,* 1 Department of Biochemistry, Medical College of Wisconsin, Milwaukee, WI 53226, USA; [email protected] 2 Medical Scientist Training Program, Medical College of Wisconsin, Milwaukee, WI 53226, USA 3 Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI 53226, USA; [email protected] * Correspondence: [email protected] (B.F.V.); [email protected] (A.R.H.) † These authors contributed equally. Abstract: Candida species cause serious infections requiring prolonged and sometimes toxic therapy. Antimicrobial proteins, such as chemokines, hold great interest as potential additions to the small number of available antifungal drugs. Metamorphic proteins reversibly switch between multiple different folded structures. XCL1 is a metamorphic, antimicrobial chemokine that interconverts between the conserved chemokine fold (an α–β monomer) and an alternate fold (an all-β dimer). Previous work has shown that human XCL1 kills C. albicans but has not assessed whether one or both XCL1 folds perform this activity. Here, we use structurally locked engineered XCL1 variants and Candida killing assays, adenylate kinase release assays, and propidium iodide uptake assays to demonstrate that both XCL1 folds kill Candida, but they do so via different mechanisms. Our results suggest that the alternate fold kills via membrane disruption, consistent with previous work, and the chemokine fold does not. XCL1 fold-switching thus provides a mechanism to regulate Citation: Dishman, A.F.; He, J.; the XCL1 mode of antifungal killing, which could protect surrounding tissue from damage associ- Volkman, B.F.; Huppler, A.R. -
Critical Roles of Chemokine Receptor CCR10 in Regulating Memory Iga
Critical roles of chemokine receptor CCR10 in PNAS PLUS regulating memory IgA responses in intestines Shaomin Hu, KangKang Yang, Jie Yang, Ming Li, and Na Xiong1 Center for Molecular Immunology and Infectious Diseases and Department of Veterinary and Biomedical Sciences, Pennsylvania State University, University Park, PA 16802 Edited by Rino Rappuoli, Novartis Vaccines, Siena, Italy, and approved September 12, 2011 (received for review January 5, 2011) Chemokine receptor CCR10 is expressed by all intestinal IgA-pro- specificIgA+ plasma cells could be maintained in the intestine for ducing plasma cells and is suggested to play an important role in a long time in the absence of antigenic stimulation (half-life > 16 positioning these cells in the lamina propria for proper IgA pro- wk), suggesting that unique intrinsic properties of the IgA- duction to maintain intestinal homeostasis and protect against producing plasma cells and intestinal environments might collabo- infection. However, interfering with CCR10 or its ligand did not rate to maintain the prolonged IgA production. However, mainte- impair intestinal IgA production under homeostatic conditions or nance of the antigen-specific IgA-producing plasma cells is during infection, and the in vivo function of CCR10 in the intestinal significantly affected by continuous presence of commensal bacte- IgA response remains unknown. We found that an enhanced ria, which induce generation of new IgA-producing plasma cells generation of IgA+ cells in isolated lymphoid follicles of intestines that replace the existing antigen-specificIgA+ cells in the intestine. offset defective intestinal migration of IgA+ cells in CCR10-KO mice, Molecular factors involved in the long-term IgA maintenance are resulting in the apparently normal IgA production under homeo- largely unknown and it is also not well understood how IgA memory static conditions and in primary response to pathogen infection. -
AG 39: Immunofluorescence Assays (PDF)
ibidi Application Guide Immunofluorescence Assays The Principle of Immunofluorescence Immunofluorescence Applied: Assays . 2 Experimental Examples . 13 Rat Hippocampal Neuron and Astrocyte Staining 14 Immunofluorescence Staining: Visualization of Endothelial Cell Junctions . 13 A Typical Workflow . 3 Immunostaining of Rat Dorsal Root Ganglionic Experiment Planning and Sample Preparation . 4 Cells and Schwann Cells . 13 Sample Fixation . 4 Adherens Junctions and Actin Cytoskeleton of Cell Permeabilization . 5 HUVECs Under Flow . 14 Blocking . 5 Mitochondria Staining of MDCK cells . 14 Primary Antibody Incubation . 5 Focal Adhesions of Differentiated Mouse Fibroblasts on an Elastic Surface . 15 Secondary Antibody Incubation . 6 Counterstain and Mounting . 7 Microscopy . 7 Troubleshooting . 8 Selected Publications Immunofluorescence C. Xu, et al. NPTX2 promotes colorectal cancer growth and liver With the ibidi Chambers . 9 metastasis by the activation of the canonical Wnt/beta-catenin pathway via FZD6. Cell Death & Disease, 2019, 10.1038/s41419- Comparison of Immunocytochemistry Protocols . 10 019-1467-7 Chambered Coverslips . 11 read abstract Kobayashi, T., et al. Principles of early human development and Channel Slides . 11 germ cell program from conserved model systems. Nature, Chamber Slides . 12 2017, 10.1038/nature22812 read abstract H. Tada et al. Porphyromonas gingivalis Gingipain-Dependently Enhances IL-33 Production in Human Gingival Epithelial Cells. PloS one, 2016, 10.1371/journal.pone.0152794 read abstract N. J. Foy, M. Akhrymuk, A. V. Shustov, E. I. Frolova and I. Frolov. Hypervariable Domain of Nonstructural Protein nsP3 of Venezuelan Equine Encephalitis Virus Determines Cell-Specific Mode of Virus Replication. Journal of Virology, 2013, 10.1128/ jvi.00720-13 read abstract .com The Principle of Immunofluorescence Assays Immunofluorescence (IF) is a powerful approach for getting insight into cellular structures and processes using microscopy . -
CX3CR1) Modulator, Attenuates Mucosal Inflammation and Reduces CX3CR11 Leukocyte Trafficking in Mice with Colitis
1521-0111/92/5/502–509$25.00 https://doi.org/10.1124/mol.117.108381 MOLECULAR PHARMACOLOGY Mol Pharmacol 92:502–509, November 2017 Copyright ª 2017 by The American Society for Pharmacology and Experimental Therapeutics E6130, a Novel CX3C Chemokine Receptor 1 (CX3CR1) Modulator, Attenuates Mucosal Inflammation and Reduces CX3CR11 Leukocyte Trafficking in Mice with Colitis Hisashi Wakita, Tatsuya Yanagawa, Yoshikazu Kuboi, and Toshio Imai Eisai Co., Ltd., Tsukuba Research Laboratories, Ibaraki (H.W., T.Y., Y.K.) and KAN Research Institute Inc., Hyogo (T.I.), Japan Received February 1, 2017; accepted August 16, 2017 Downloaded from ABSTRACT The chemokine fractalkine (CX3C chemokine ligand 1; CX3CL1) (IC50 4.9 nM), most likely via E6130-induced down-regulation of and its receptor CX3CR1 are involved in the pathogenesis of CX3CR1 on the cell surface. E6130 had agonistic activity via several diseases, including inflammatory bowel diseases such as CX3CR1 with respect to guanosine 59-3-O-(thio)triphosphate Crohn’s disease and ulcerative colitis, rheumatoid arthritis, hepa- binding in CX3CR1-expressing Chinese hamster ovary K1 titis, myositis, multiple sclerosis, renal ischemia, and athero- (CHO-K1) membrane and had no antagonistic activity. Orally sclerosis. There are no orally available agents that modulate the administered E6130 ameliorated several inflammatory bowel molpharm.aspetjournals.org fractalkine/CX3CR1 axis. [(3S,4R)-1-[2-Chloro-6-(trifluoromethyl) disease–related parameters in a murine CD41CD45RBhigh benzyl]-3-{[1-(cyclohex-1-en-1-ylmethyl)piperidin-4-yl]carbamoyl}- T-cell-transfer colitis model and a murine oxazolone-induced 4-methylpyrrolidin-3-yl]acetic acid (2S)-hydroxy(phenyl)acetate colitis model. -
116588NCJRS.Pdf
If you have issues viewing or accessing this file contact us at NCJRS.gov. " "'- u.s. Department of Justice Federal Bureau of Investigation PROCEEDINGS OF THE INTERNATIONAL SYMPOSIUM ON FORENSIC IMMUNOLOGY FBI ACADEMY QUANTICO, VIRGINIA JUNE 23-26, 1986 Proceedings of the International Symposium on Forensic Immunology co 00 L() \0 u, r-l O§ r-l Ql C. If) 05~ Ql 0- 0 ~ o~ Ql E C/) Ql >. c:0 If) C/) ~ * ....,a: () a: z Ql '*02 Ql iii :5 ...... ....,::> a Ql {ij "...:0- Ql c: !!lc: °E ::>;: B 00 {ij c: 0 ~I::> z~ "e CD ~~ :5 .... ~o- S 1::C: Lt .~ Host Laboratory Division Federal Bureau of Investigation June 23-26, 1986 Forensic Science Research and Training Center FBI Academy Quantico, Virginia NOTICE This publication was prepared by the U. S. Government. Neither the U. S. Government nor the U. S. Department of Justice nor any of their employees makes any warranty, express or implied, or assumes any legal liability or responsibility for the accuracy, completeness or usefulness of any information, apparatus, product or process disclosed, or represents that in use would not infringe privately owned rights. Reference herein to any specific commercial product, process or service by trade name, mark, manufacturer or otherwise does not necessarily constitute or imply its endorsement, recommendation or favoring by the U. S. Government or any agency thereof. The views and opinions of authors expressed herein do not necessarily state or reflect those of the U. S. Government or any agency thereof. Published by: The Laboratory Division Roger T. Castonguay Assistant Director in Charge Federal Bureau of Investigation U. -
CCL20/CCR6 Signaling Regulates Bone Mass Accrual in Mice
ORIGINAL ARTICLE JBMR CCL20/CCR6 Signaling Regulates Bone Mass Accrual in Mice Michele Doucet, Swaathi Jayaraman, Emily Swenson, Brittany Tusing, Kristy L Weber,Ã and Scott L Kominsky Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA ABSTRACT CCL20 is a member of the macrophage inflammatory protein family and is reported to signal monogamously through the receptor CCR6. Although studies have identified the genomic locations of both Ccl20 and Ccr6 as regions important for bone quality, the role of CCL20/CCR6 signaling in regulating bone mass is unknown. By micro–computed tomography (mCT) and histomorphometric analysis, we show that global loss of Ccr6 in mice significantly decreases trabecular bone mass coincident with reduced osteoblast numbers. Notably, CCL20 and CCR6 were co-expressed in osteoblast progenitors and levels increased during osteoblast differentiation, indicating the potential of CCL20/CCR6 signaling to influence osteoblasts through both autocrine and paracrine actions. With respect to autocrine effects, CCR6 was found to act as a functional G protein–coupled receptor in osteoblasts and although its loss did not appear to affect the number or proliferation rate of osteoblast progenitors, differentiation was significantly inhibited as evidenced by delays in osteoblast marker gene expression, alkaline phosphatase activity, and mineralization. In addition, CCL20 promoted osteoblast survival concordant with activation of the PI3K-AKT pathway. Beyond these potential autocrine effects, osteoblast-derived CCL20 stimulated the recruitment of macrophages and T cells, known facilitators of osteoblast differentiation and survival. Finally, we generated mice harboring a global deletion of Ccl20 and found that Ccl20-/- mice exhibit a reduction in bone mass similar to that observed in Ccr6-/- mice, confirming that this phenomenon is regulated by CCL20 rather than alternate CCR6 ligands. -
CCBP2 293 Cell Lysate Storage: Store at -80°C
From Biology to Discovery™ CCBP2 293 Cell Lysate Storage: Store at -80°C. Minimize freeze-thaw cycles. After addition of 2X SDS Loading Buffer, the lysates can be stored Subcategory: Cell Lysate at -20°C. Product is guaranteed 6 months from the date of Cat. No.: 400521 shipment. Unit: 0.1 mg For research use only, not for diagnostic or therapeutic Description: procedures. Antigen standard for chemokine binding protein 2 (CCBP2) is a lysate prepared from HEK293T cells transiently transfected with a TrueORF gene-carrying pCMV plasmid (OriGene Technologies, Inc.) and then lysed in RIPA Buffer. Protein concentration was determined using a colorimetric assay. The antigen control carries a C-terminal Myc/DDK tag for detection. Applications: ELISA, WB, IP Format: This product includes 3 vials: 1 vial of gene-specific cell lysate, 1 vial of control vector cell lysate, and 1 vial of loading buffer. Each lysate vial contains 0.1 mg lysate in 0.1 ml (1 mg/ml) of RIPA Buffer (50 mM Tris-HCl pH7.5, 250 mM NaCl, 5 mM EDTA, 50 mM NaF, 1% NP40). The loading buffer vial contains 0.5 ml 2X SDS Loading Buffer (125 mM Tris-Cl, pH6.8, 10% glycerol, 4% SDS, 0.002% Bromophenol blue, 5% beta-mercaptoethanol). Alternate Names: CC-chemokine-binding receptor JAB61; chemokine (C-C) receptor 9; chemokine (C-C motif) receptor 9; chemokine receptor D6; chemokine receptor CCR-9; C-C chemokine receptor D6; chemokine receptor CCR-10; chemokine-binding protein D6; CCBP2; CCR10; CCR9; CMKBR9; D6; hD6; MGC126678; MGC138250 Accession No.: NP_001287 Application Notes: WB: Mix equal volume of lysates with 2X SDS Loading Buffer.