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Product Name
Anti-MCP-3/CCL7 antibody
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Description
Mouse monoclonal to MCP-3/CCL7
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Tested applications
ELISA, IF, ICC/IF
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Species reactivity
Human CCL7 / MCP3
No cross-reactivity in ELISA with E.coli cell lysate -
Alternative names
Ccl7 antibody; MARC antibody; marc antibody; mcp3 antibody; MCP3 antibody; MCP-3 antibody; MCP-3 antibody; MGC138465 antibody; NC28 antibody; RP23-350G1.4 antibody; SCYA7 antibody; CCL7 antibody; FIC antibody; fic antibody; MGC138463 antibody; SCYA6 antibody; Scya7 antibody; FIC antibody; MARC antibody; MCP3 antibody; NC28 antibody; MCP-3 antibody; SCYA6 antibody; SCYA7 antibody; fic antibody; marc antibody; mcp3 antibody; MCP-3 antibody; Scya7 antibody
- Immunogen
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Isotype
Mouse IgG1
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Preparation
This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human CCL7 / MCP3 (rh CCL7 / MCP3; NP_006264.2; Gln 24-Leu 99). The IgG fraction of the cell culture supernatant was purified by Protein A affinity chromatography.
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Clonality
Monoclonal
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Formulation
0.2 μm filtered solution in PBS with 5% trehalose
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Storage instructions
This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free.
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles. -
Applications
ELISA: 0.5-1 μg/mL
This antibody can be used at 0.5-1 μg/mL with the appropriate secondary reagents to detect Human CCL7. The detection limit for Human CCL7 is approximately 0.0195 ng/well.
ICC/IF: 10-25 μg/mL
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Validations
MCP-3 / CCL7 Antibody, Mouse MAb, Immunofluorescence
Immunofluorescence staining of Human CCL7 in SKBR3 cells. Cells were fixed with 4% PFA, permeabilzed with 1% Triton X-100 in PBS, blocked with 10% serum, and incubated with Mouse anti-Human CCL7 monoclonal antibody (15 µg/ml). Then cells were stained with the Alexa Fluor® 488-conjugated Goat Anti-mouse IgG secondary antibody (left panel, captured by laser confocal scanning microscope; right panel, captured by fluorescence microscope), countstained with DAPI (blue). Positive staining was localized to cytoplasm.
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Background
Chemokines are a family of small chemotactic cytokines, or proteins secreted by cells. Chemokines share the same structure similarities such as small size, and the presence of four cysteine residues in conserved locations in order to form their 3-dimensional shape. Some of the chemokines are considered pro-inflammatory which can be induced to recruit cells of the immune system to a site of infection during an immune response, while others are considered homeostatic and are implied in controlling the migration of cells during normal processes of tissue maintenance and development. There are four members of the chemokine family: C-C kemokines, C kemokines, CXC kemokines and CX3C kemokines. The C-C kemokines have two cysteines nearby the amino terminus. There have been at least 27 distinct members of this subgroup reported for mammals, called C-C chemokine ligands-1 to 28. Chemokine ligand 7(CCL7), also known as MCP-3, is a isform of the C-C chemokine subfamily of the chemokine family which is produced by certain tumor cells and by macrophages. It also own two adjacent N-terminal cysteine residues. Chemokine ligand 7(CCL7) spacifically attracts monocytes, and regulates macrophage function.
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References
- Laing KJ, et al. (2004) Chemokines. Developmental and comparative immunology. 28(5): 443-60.
- Cocchi F, et al. (1995) Identification of RANTES, MIP-1a, and MIP-1b as the major HIV-suppressive factor produced by CD8+ T cells. Science. 270 (5243): 1811-5.
- Michalec L, et al. (2002) CCL7 and CXCL10 Orchestrate Oxidative Stress-Induced Neutrophilic Lung Inflammation. The Journal of Immunology. 168: 846-52.
- Wetzel K,et al. (2007) MCP-3 (CCL7) delivered by parvovirus MVMp reduces tumorigenicity of mouse melanoma cells through activation of T lymphocytes and NK cells.International Journal of Cancer. 120(6):1364-71.
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