Anti-CCL6 monoclonal antibody [Biotin] (DCABY-4321)

Rat Anti-Mouse CCL6 monoclonal antibody for ELISA(Det)

Specifications


Host Species
Rat
Antibody Isotype
IgG2a
Clone
373009
Species Reactivity
Mouse
Immunogen
E. coli-derived recombinant mouse CCL6/C10. Gly22-Ala116 Accession Number P27784
Conjugate
Biotin

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

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References


Pulmonary chemokine expression is coordinately regulated by STAT1, STAT6, and IFN-gamma

JOURNAL OF IMMUNOLOGY

Authors: Fulkerson, PC; Zimmermann, N; Hassman, LM; Finkelman, FD; Rothenberg, ME

The expression of distinct chemokines within the asthmatic lung suggests that specific regulatory mechanisms may mediate various stages of asthmatic disease. Global transcript expression profiling was used to define the spectrum and kinetics of chemokine involvement in an experimental murine model of asthma. Seventeen chemokines were induced in the lungs of allergen-inoculated mice, as compared with saline-treated mice. Two (CXCL13 and CCL9) of the 17 identified chemokines have not previously been associated with allergic airway disease. Seven (7 of 17; CCL2, CCL7, CCL9, CCL11, CXCL1, CXCL5, CXCL10) of the allergen-induced chemokines were induced early after allergen challenge and remained induced throughout the experimental period. Three chemokines (CXCL2, CCL3, and CCL17) were induced only during the early phase of the inflammatory response after the initial allergen challenge, while seven chemokines (CCL6, CCL8, CCL12, CCL22, CXCL9, CXCL12, and CXCL13) were increased only after a second allergen exposure. Unexpectedly, expression of only three chemokines, CCL11, CCL17, and CCL22, was STAT6 dependent, and many of the identified chemokines were overexpressed in STAT6-deficient mice, providing an explanation for the enhanced neutrophilic inflammation seen in these mice. Notably, IFN-gamma and STAT1 were shown to contribute to the induction of two STAT6-independent chemokines, CXCL9 and CXCL10. Taken together, these results show that only a select panel of chemokines (those targeting Th2 cells and eosinophils) is positively regulated by STAT6; instead, many of the allergen-induced chemokines are negatively regulated by STAT6. Collectively, we demonstrate that allergen-induced inflammation involves coordinate regulation by STAT1, STAT6, and IFN-gamma.

Raloxifene and Antiestrogenic Gonadorelin Inhibits Intestinal Tumorigenesis by Modulating Immune Cells and Decreasing Stem-like Cells

CANCER PREVENTION RESEARCH

Authors: Janakiram, Naveena B.; Mohammed, Altaf; Brewer, Misty; Bryant, Taylor; Biddick, Laura; Lightfoot, Stan; Pathuri, Gopal; Gali, Hariprasad; Rao, Chinthalapally V.

Studies suggest that estrogen plays a contributing role in colorectal cancer. This project examined the preventive effects of raloxifene, a selective estrogen receptor modulator (SERM), and gonadorelin, an antiestrogenic drug, in female Apc(Min/+) mouse intestinal tumorigenesis. Six-week-old Apc(Min/+) mice were fed diet containing 1 ppm raloxifene or control diet. Gonadorelin (150 ng/mouse) was injected subcutaneously into one treatment group. Intestinal tumors were evaluated for tumor multiplicity and size. Mice treated with raloxifene and gonadorelin showed colon tumor inhibition of 80% and 75%, respectively. Both drugs significantly inhibited small intestinal tumor multiplicity and size (75%-65%, P < 0.0001). Raloxifene and gonadorelin showed significant tumor inhibition with 98% and 94% inhibition of polyps > 2 mm in size. In mice fed with raloxifene or injected with gonadorelin, tumors showed significantly reduced proliferating cell nuclear antigen expression (58%-65%, P < 0.0001). Raloxifene treatment decreased beta-catenin, cyclin D1, laminin 1 beta, Ccl6, and stem-like cells (Lgr 5, EpCAM, CD44/CD24), as well as suppressed inflammatory genes (COX-2, mPGES-1, 5-LOX,). Gonadorelin showed significant decrease in COX-2, mPGES-1, iNOS, and stem-like cells or increased NK cells and chemokines required for NK cells. Both drugs were effective in suppressing tumor growth albeit with different mechanisms. These observations show that either suppression of estrogen levels or modulation of estrogen receptor dramatically suppresses small intestinal and colonic tumor formation in female Apc(Min/+) mice. These results support the concept of chemoprevention by these agents in reducing endogenous levels of estrogen or modulating ER signaling. (C) 2014 AACR.

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