Anti-CCL6 monoclonal antibody (DCABY-4208)

Specifications


Host Species
Rat
Antibody Isotype
IgG2a
Clone
373026
Species Reactivity
Mouse
Immunogen
E. coli-derived recombinant mouse CCL6/C10. Gly22-Ala116 Accession Number P27784
Conjugate
Unconjugated

Applications


Application Notes
ELISA Capture: 2-8 μg/mL; ELISA Detection: 0.5-2 μg/mL
We recommend the following for sandwich ELISA (Capture - Detection):
DCABY-4208 - DCABY-4321
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.

Target


Alternative Names
CCL6; chemokine (C-C motif) ligand 6; c10; MRP-1; Scya6; C-C motif chemokine 6
Entrez Gene ID
UniProt ID

Product Background


Pathway
Chemokine signaling pathway; Class A/1 (Rhodopsin-like receptors); Cytokine-cytokine receptor interaction; Formyl peptide receptors bind formyl peptides and many other ligands; G alpha (i) signalling events; G alpha (q) signalling events; GPCR downstream

Citations


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Custom Antibody Labeling


We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

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References


Gene expression profiles reveal increased mClca3 (Gob5) expression and much production in a murine model of asbestos-induced fibrogenesis

AMERICAN JOURNAL OF PATHOLOGY

Authors: Sabo-Attwood, T; Ramos-Nino, M; Bond, J; Butnor, KJ; Heintz, N; Gruber, AD; Steele, C; Taatjes, DJ; Vacek, P; Mossman, BT

To elucidate genes important in development or repair of asbestos-induced lung diseases, gene expression was examined in mice after inhalation of chrysotile asbestos for 3, 9, and 40 days. We identified changes in the expression of genes linked to proliferation (cyclin B2, CDC20, and CDC28 protein kinase regulatory subunit 2), inflammation (CCL9, CCL6, complement component 1, chitinase3-like 3, TNF superfamily member 10, and IL-1B), and matrix remodeling (MMP12, MMP3, integrin alpha X, and cathepsins K, Z, B, and S). The most highly induced gene at all time points was mclca3 (gob5), a putative calcium-activated chloride channel involved in the regulation of mucus production and/or secretion. Using histochemistry, we demonstrated accumulation of mucus and increased mClca3 protein in the bronchiolar epithelium of asbestos-exposed mice at all time points but peaking at 9 days. Cytokine levels (interleukin-1 beta, interleukin-4, interleukin-6) in bronchoalveolar lavage fluid also increased at 9 days, suggesting Th2-mediated immunity may play a role in asbestos-induced mucus production. In contrast, levels of cathepsin K, a potent elastase, increased between 3 and 40 days at both the mRNA and protein levels, localizing primarily in CD45-positive leukocytes and interstitial cells. Identification of genes involved in lung injury and remodeling after asbestos exposure could aid in defining mechanisms of airborne particulate-induced disease and in developing therapeutic strategies.

Murine lung eosinophil activation and chemokine production in allergic airway inflammation

CELLULAR & MOLECULAR IMMUNOLOGY

Authors: Rose, C. Edward, Jr.; Lannigan, Joanne A.; Kim, Paul; Lee, James J.; Fu, Shu Man; Sung, Sun-sang J.

Eosinophils play important roles in asthma and lung infections. Murine models are widely used for assessing the functional significance and mechanistic basis for eosinophil involvements in these diseases. However, little is known about tissue eosinophils in homeostasis. In addition, little data on eosinophil chemokine production during allergic airway inflammation are available. In this study, the properties and functions of homeostatic and activated eosinophils were compared. Eosinophils from normal tissues expressed costimulation and adhesion molecules B7-1, B7-2 and ICAM-1 for Ag presentation but little major histocompatibility complex (MHC) class II, and were found to be poor stimulators of T-cell proliferation. However, these eosinophils expressed high levels of chemokine mRNA including C10, macrophage inflammatory protein (MIP)-1 alpha, MIP-1 gamma, MIP-2, eotaxin and monocyte chemoattractant protein-5 (MCP-5), and produced chemokine proteins. Eosinophil intracellular chemokines decreased rapidly with concomitant surface marker downregulation upon in vitro culturing consistent with piecemeal degranulation. Lung eosinophils from mice with induced allergic airway inflammation exhibited increased chemokines mRNA expression and chemokines protein production and upregulated MHC class II and CD11c expression. They were also found to be the predominant producers of the CCR1 ligands CCL6/C10 and CCL9/MIP-1 gamma in inflamed lungs. Eosinophil production of C10 and MIP-1 gamma correlated with the marked influx of CD11b(high) lung dendritic cells during allergic airway inflammation and the high expression of CCR1 on these dendritic cells (DCs). The study provided baseline information on tissue eosinophils, documented the upregulation of activation markers and chemokine production in activated eosinophils, and indicated that eosinophils were a key chemokine-producing cell type in allergic lung inflammation. Cellular & Molecular Immunology (2010) 7, 361-374; doi:10.1038/cmi.2010.31; published online 12 July 2010

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