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RnDSy-lu-2945 Products for Chemokine Research The Chemokine Superfamily Chemokines are small cell surface-localized or secreted chemotactic cytokines that bind to and activate specific G protein-coupled chemokine receptors. Most chemokines have at least four conserved N-terminal cysteine residues that form two intramolecular disulfide bonds. Four chemokine subfamilies (CXC, CC, C and CX3C) have been defined based upon the placement of the first two cysteine residues. The CXC chemokine subfamily is characterized by two cysteine residues separated by one amino acid. Within this subfamily, two CXC classes are further defined by the presence or absence of an ELR motif sequence. ELR– CXC chemokines act as chemoattractants for lymphocytes, while ELR+ CXC chemokines are chemoattractants for neutrophils. Additionally, CXC chemokines can mediate angiogenesis.1 The CC chemokine subfamily is defined by two adjacent cysteine CCR1 H: CCL3-5, 7, 8, 13-16, 23, CCL3L1, CCL3L3, CCL4L1, CCL4L2 M: CCL3-7, 9/10 residues. CC chemokines induce inflammatory H: XCL1, 2 XCR1 responses via regulation of monocyte, M: XCL1 macrophage, mast cell, and T cell migration.2 H: CCL2, 7, 8, 13, 16 CCR2 (A or B) M: CCL2, 7, 12 C chemokines are characterized by a single H: CCL26 CX3CR1 cysteine residue and are constitutively expressed H: CX3CL1 in the thymus where they regulate T cell H: CCL5, 7, 8, 11, 13, 14, 15, 24, 26, 28, CCL3L1, CCL3L3 M: CX3CL1 CCR3 M: CCL5, 7, 9/10, 11, 24 differentiation.3 The CX3C chemokine subfamily is defined by two cysteine residues separated by H: CXCL6-8 CXCR1 three amino acids. Cell surface-localized CX3CL1/ H: CCL2, 3, 5, 17, 22 M: CXCL7, LIX CCR4 Fractalkine mediates leukocyte adhesion while M: CCL2, 3, 5, 17, 22 soluble CX3CL1/Fractalkine is chemotactic for H: CXCL1-3, 5-8 leukocytes.4 CX3CL1/Fractalkine is also a critical H: CCL3-5, 8, 11, 13, 14, 16, CCL3L1, M: CXCL1-3, 7, LIX CXCR2 CCR5 CCL3L3, CCL4L1, CCL4L2 regulator of microglia-neuron communication M: CCL3-5 during neural development.5 H: CXCL4, 9-11, 13, CXCL4L1 While chemokine receptors generally bind only CCR6 H: CCL20 M: CXCL4, 9-11 CXCR3 M: CCL20 one subfamily of chemokines, within those subfamilies, most chemokines display promiscuous receptor binding patterns. The CCR7 H: CCL19, 21 M: CCL19, 21 H: CXCL4, 9-11, CXCL4L1 CXCR3B redundancy of chemokine ligand-receptor binding may ensure robust signaling. In addition, promiscuous binding and non-signaling CCR8 H: CCL1, 4, 16, 17 M: CCL1, 8 H: CXCL12 CXCR4 chemokine receptors offer mechanisms by which M: CXCL12 chemokine signaling can be regulated by either subtle differences in receptor signaling or H: CCL25 CCR9 M: CCL25 differences in ligand-receptor expression H: CXCL13 M: CXCL13 CXCR5 patterns.6 Select chemokine ligands and receptors are implicated in HIV infection and H: CCL27, 28 CCR10 M: CCL27, 28 persistence, while aberrant chemokine H: CXCL16 expression and signaling is associated with M: CXCL16 CXCR6 pathological conditions including inflammatory CCR11 H: CCL2, 8, 13, 19, 21, 25 diseases and cancer.7-9 M: CCL19, 21, 25 References H: CXCL11, 12 CXCR7 1. Mehrad, B. et al. (2007) Thromb. Haemost. 97:755. M: CXCL11, 12 PITPNM3 H: CCL18 2. Ono, S.J. et al. (2003) J. Allergy Clin. Immunol. 111:1185. 3. Lei, Y. & Y. Takahama (2012) Microbes Infect. 14:262. H: CXCL14, 17 4. Jones, B.A. et al. (2010) Mol. Interv. 10:263. M: CXCL14, 17 Unknown 5. Wolf, Y. et al. (2013) Front. Cell. Neurosci. 7:26. CCRL2/CRAM-A/B H: CCL19 M: CXCL15 6. Bennett, L.D. et al. (2011) Immunology 134:246. 7. Evans, V.A. et al. (2012) Cytokine Growth Factor Rev. 23:151. 8. Balkwill, F.R. (2012) J. Pathol. 226:148. H: CCL1, 2, 5, 7, 8, 11, 13, 14, 16-18 9. White, G.E. et al. (2013) Pharmacol. Rev. 65:47. CCRL2/LCCR M: CCL19 M: CCL2, 11 H: CXCL1-3, 5, 6, 8 DARC M: CXCL1, 2, LIX H: CXCL4, 9-11, 13 D6 H: CCL2-5, 7, 8, 11, 13, 14, 17, 22, CCL3L1 M: CCL2, 3 Key H: Human M: Mouse C Chemokines/Receptors CXC ELR+ Chemokines/Receptors For additional information CC Chemokines/Receptors CX3C Chemokines/Receptors >RnDSystems.com/ChemokineInfoTable CXC ELR- Chemokines/Receptors Non-signaling Chemokine Receptors CXC Chemokines CXC Chemokines Recombinant & Recombinant CXC chemokines, also known as α chemokines, Molecule Natural Proteins Antibodies ELISAs Human Protein Sampler Packs are critical regulators of normal development CXCL1/2/3/GRO CR H (B/N, FC, WB) CR (B/N, WB) and immune responses. The CXC chemokine subfamily consists of nineteen ligands and H (B/N, E, FC, WB) M (B/N, E, WB) CXCL1/GROα/KC/CINC-1 H M R H M R R (B/N, IHC, WB) seven receptors. CXC chemokines that contain an ELR motif are potent angiogenic H (B/N, FC, WB) M (B/N, E, ICC, IHC, WB) CXCL2/GROβ/MIP-2/CINC-3 H M R CR M R factors, while ELR–CXC chemokines are R (B/N, E, WB) angiostatic. Select CXC chemokines and CXCL3/GROγ/CINC-2/DCIP-1 H M R H (B/N, FC, WB) M (B/N, WB) R (B/N, E, WB) R receptors regulate hematopoietic stem cell CXCL4/PF4 H M H (E, FC, WB) M (E, WB) H M migration. They are also involved in regulating CXCL5/ENA-70 H tumor progression and are of interest as targets 1-3 CXCL5/ENA-74 H for therapeutic intervention. References CXCL5/ENA-78 H H (B/N, E, FC, IHC, WB) H 1. Zhu, Q. et al. (2012) J. Mol. Histol. 43:699. CXCL6/GCP-2 H H (B/N, E, FC, WB) H 2. Vinader, V. & K. Afarinkia (2012) Future Med. Chem. 4:853. CXCL7/NAP-2 H H (B/N, E, WB) H 3. Owen, J.L. & M. Mohamadzadeh (2013) Front. Physiol. 4:159. CXCL7/Thymus Chemokine-1 M R M (B/N, E, IHC, WB) R (B/N, E, IHC, WB) M R 104 H (B/N, E, FC, ICC, IHC, WB) P (B/N, E, WB) CXCL8/IL-8 H P Ca F H P Ca F Ca (B/N, E, ICC, WB) F (B/N, E, ICC, WB) 103 CXCL9/MIG H M H (B/N, E, FC, ICC, WB) M (B/N, E, WB) H M H (B/N, E, FC, ICC, WB) M (B/N, E, IHC, WB) CXCL10/IP-10/CRG-2 H M CR H M CR (B/N, WB) 102 CXCL11/I-TAC H M H (B/N, E, WB) M (B/N, E, WB) H M CXCR5 CXCL12/SDF-1 H M F RM H (B/N, E, FC, IHC, WB) M (B/N, E, FC, IHC, WB) H M 1 CXCL12/SDF-1α H M F RM H M 10 CXCL12/SDF-1β H F H (B/N, E, WB) CXCL12/SDF-1γ H 100 CXCL13/BLC/BCA-1 H M H (B/N, E, FC, IHC, WB) M (B/N, E, IHC, WB) H M 100 101 102 103 104 B220/CD45R CXCL14/BRAK H M H (E, WB) M (WB) H Detection of CXCR5 and B220/CD45R on Mouse Splenocytes by Flow CXCL15/Lungkine M M (E, WB) M Cytometry. Mouse splenocytes were stained for CXCR5 and B220/CD45R expression using a PE-conjugated Rat Anti-Mouse CXCR5 Monoclonal Anti- CXCL16 H M H (B/N, E, FC, IHC, WB) M (B/N, E, FC, WB) H M body (Catalog # FAB6198P) and an APC-conjugated Rat Anti-Mouse B220/ CXCL17/VCC-1 H M H (FC, ICC, WB) M (WB) CD45R Monoclonal Antibody (Catalog # FAB1217A). Quadrants were set based on isotype controls. LIX M R M (B/N, E, WB) R (B/N, E, WB) M R CXCR1/IL-8 RA Antibody (µg/mL) 10-2 10-1 100 101 CXC Chemokine Receptors 6000 6000 Molecule Antibodies Tocris Biochemicals & Peptides 5000 5000 CXCR1/IL-8 RA H (B/N, FC, IHC) (Mean RFU) Migration Cell CXCR2/IL-8 RB H (B/N, FC, IHC) M (B/N, FC) 4000 4000 CXCR3 H (B/N, FC, IHC) M (FC) 3000 3000 CXCR4 H (B/N, FC, IHC) M (B/N, FC, ICC, IHC) F (FC, ICC) CXCR5 H (B/N, FC, ICC, IHC) M (FC, ICC) 2000 2000 Cell Migration (Mean RFU) Migration Cell CXCR6 H (FC) M (FC) 1000 1000 CXCR7/RDC-1 H (FC, IHC) M (FC, WB) DARC H (FC, ICC) M (FC, WB) R (FC, WB) 0 0 10-2 10-1 100 101 CXCL8/IL-8 (ng/mL) Species Key: H Human, M Mouse, R Rat, B Bovine, Ca Canine, CR Cotton Rat, F Feline, P Porcine, RM Rhesus Macaque, V Viral Chemotaxis Induced by CXCL8/IL‑8 and Neutralization using a Human Application Key: B/N Blocking/Neutralization, E ELISA (Cap. or Det.), FC Flow Cytometry, ICC Immunocytochemistry, IHC Immunohistochemistry, IP Immunoprecipitation, CXCR1/IL‑8 RA Antibody. Recombinant Human CXCL8/IL-8 (Catalog # WB Western Blot 208-IL) chemoattracts the BaF3 mouse pro-B cell line transfected with hu- man CXCR1/IL-8 RA in a dose-dependent manner (orange line). The amount of cells that migrated through to the lower chemotaxis chamber was mea- sured by Resazurin (Catalog # AR002). Chemotaxis elicited by 1 ng/mL Recombinant Human CXCL8/IL-8 was neutralized by increasing concentra- tions of Human CXCR1/IL-8 RA Monoclonal Antibody (Catalog # MAB330; green line). Learn more | rndsystems.com/chemokines CC Chemokines CC Chemokines Recombinant CC chemokines, also known as β chemokines, Molecule Recombinant & Antibodies ELISAs Human Protein are critical mediators of the inflammatory Natural Proteins Sampler Packs response.
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  • Acting on the CCR1 Receptor Mediates Neutrophil Migration in Immune Inflammation Via Sequential ␣ Release of TNF- and LTB4 Cleber D

    Acting on the CCR1 Receptor Mediates Neutrophil Migration in Immune Inflammation Via Sequential ␣ Release of TNF- and LTB4 Cleber D

    MIP-1␣[CCL3] acting on the CCR1 receptor mediates neutrophil migration in immune inflammation via sequential ␣ release of TNF- and LTB4 Cleber D. L. Ramos,* Claudio Canetti,*,† Janeusa T. Souto,‡,§ Joa˜ o S. Silva,‡ Cory M. Hogaboam,¶ Sergio H. Ferreira,* and Fernando Q. Cunha*,1 Departments of *Pharmacology and ‡Biochemistry and Immunology, School of Medicine of Ribeira˜o Preto, University of Sa˜o Paulo, Brazil; §Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, RN, Brazil; and †Division of Pulmonary & Critical Care Medicine and ¶Department of Pathology, University of Michigan, Ann Arbor Abstract: In the present study, we investigated nists might have a therapeutic potential. J. Leukoc. the involvement of macrophage-inflammatory pro- Biol. 78: 167–177; 2005. tein-1␣ (MIP-1␣)[CC chemokine ligand 3 (CCL3)], MIP-1␤[CCL4], regulated on activation, normal Key Words: chemokines ⅐ chemokine receptors ⅐ chemotaxis T expressed and secreted (RANTES)[CCL5], and CC chemokine receptors (CCRs) on neutrophil mi- gration in murine immune inflammation. Previ- INTRODUCTION ously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor Neutrophil migration is a complex process, which results ␣ ␣ mainly from the release of neutrophil chemotactic factors by (TNF- ) and leukotriene B4 (LTB4). Herein, we show increased mRNA expression for MIP- resident cells, inducing rolling and adhesion of neutrophils on 1␣[CCL3], MIP-1␤[CCL4], RANTES[CCL5], and endothelial cells, followed by their transmigration to the ex- travascular space [1, 2]. Apart from its importance in host CCR1 in peritoneal cells harvested from OVA-chal- defense, the migration of neutrophils to the inflammatory site lenged, immunized mice, as well as MIP-1␣[CCL3] is, at least in part, responsible for tissue damage observed in and RANTES[CCL5] but not MIP-1␤[CCL4] proteins several inflammatory diseases such as rheumatoid arthritis, in the peritoneal exudates.
  • Mechanism of Macrophage-Derived Chemokine/CCL22 Production by Hacat Keratinocytes

    Mechanism of Macrophage-Derived Chemokine/CCL22 Production by Hacat Keratinocytes

    C Yano, et al Ann Dermatol Vol. 27, No. 2, 2015 http://dx.doi.org/10.5021/ad.2015.27.2.152 ORIGINAL ARTICLE Mechanism of Macrophage-Derived Chemokine/CCL22 Production by HaCaT Keratinocytes Chizuko Yano, Hidehisa Saeki1, Mayumi Komine2, Shinji Kagami3, Yuichiro Tsunemi4, Mamitaro Ohtsuki2, Hidemi Nakagawa Department of Dermatology, The Jikei University School of Medicine, 1Department of Dermatology, Nippon Medical School, Tokyo, 2Department of Dermatology, Jichi Medical University, Shimotsuke, 3Department of Dermatology, Kanto Central Hospital, 4Department of Dermatology, Tokyo Women’s Medical University, Tokyo, Japan Background: CC chemokine ligand 17 (CCL17) and CCL22 27(2) 152∼156, 2015) are the functional ligands for CCR4. We previously reported that inhibitors of nuclear factor-kappa B and p38 mi- -Keywords- togen-activated protein kinase (p38 MAPK), but not of ex- Chemokine CCL22, Chemokine CCL17, Epidermal growth tracellular signal-related kinase (ERK), inhibited tumor ne- factor receptor, HaCaT keratinocytes crosis factor (TNF)-α- and interferon (IFN)-γ-induced pro- duction of CCL17 by the human keratinocyte cell line, HaCaT. Further, an inhibitor of epidermal growth factor re- INTRODUCTION ceptor (EGFR) enhanced the CCL17 production by these keratinocytes. Objective: To identify the mechanism under- The macrophage-derived chemokine (MDC)/CC chemo- lying CCL22 production by HaCaT cells. Methods: We inves- kine ligand 22 (CCL22) is one of the functional ligands for tigated the signal transduction pathways by which TNF-α CC chemokine receptor 4 (CCR4) and is a chemoattractant and IFN-γ stimulate HaCaT cells to produce CCL22 by add- for the CCR4-expressing cells such as Th2 cells. We and ing various inhibitors.
  • Bioinformatics Identification of CCL8/21 As Potential Prognostic

    Bioinformatics Identification of CCL8/21 As Potential Prognostic

    Bioscience Reports (2020) 40 BSR20202042 https://doi.org/10.1042/BSR20202042 Research Article Bioinformatics identification of CCL8/21 as potential prognostic biomarkers in breast cancer microenvironment 1,* 2,* 3 4 5 1 Bowen Chen , Shuyuan Zhang ,QiuyuLi, Shiting Wu ,HanHe and Jinbo Huang Downloaded from http://portlandpress.com/bioscirep/article-pdf/40/11/BSR20202042/897847/bsr-2020-2042.pdf by guest on 28 September 2021 1Department of Breast Disease, Maoming People’s Hospital, Maoming 525000, China; 2Department of Clinical Laboratory, Maoming People’s Hospital, Maoming 525000, China; 3Department of Emergency, Maoming People’s Hospital, Maoming 525000, China; 4Department of Oncology, Maoming People’s Hospital, Maoming 525000, China; 5Department of Medical Imaging, Maoming People’s Hospital, Maoming 525000, China Correspondence: Shuyuan Zhang ([email protected]) Background: Breast cancer (BC) is the most common malignancy among females world- wide. The tumor microenvironment usually prevents effective lymphocyte activation and infiltration, and suppresses infiltrating effector cells, leading to a failure of the host toreject the tumor. CC chemokines play a significant role in inflammation and infection. Methods: In our study, we analyzed the expression and survival data of CC chemokines in patients with BC using several bioinformatics analyses tools. Results: The mRNA expression of CCL2/3/4/5/7/8/11/17/19/20/22 was remark- ably increased while CCL14/21/23/28 was significantly down-regulated in BC tis- sues compared with normal tissues. Methylation could down-regulate expression of CCL2/5/15/17/19/20/22/23/24/25/26/27 in BC. Low expression of CCL3/4/23 was found to be associated with drug resistance in BC.