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ABF119

Sigma-Aldrich

Anti-CLEC7A (Dectin-1) Antibody

from rabbit, purified by affinity chromatography

Synonym(s):

CLEC7A, C-type lectin domain family 7 member A, Beta-glucan receptor, C-type lectin superfamily member 12, Dendritic cell-associated C-type lectin 1, DC-associated C-type lectin 1, Dectin-1

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

rabbit

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

purified by

affinity chromatography

species reactivity

mouse, rat, human

species reactivity (predicted by homology)

baboon (based on 100% sequence homology), primate (based on 100% sequence homology)

technique(s)

flow cytometry: suitable
western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

ambient

Gene Information

human ... CLEC7A(64581)

General description

C-type lectin domain family 7 member A (CLEC7A), also known as Dendritic cell-associated C-type lectin 1 (Dectin-1), is a member of our innate immunity receptor family of proteins that serves as a receptor for important glycopolymers. CLEC7A is the receptor for beta glycans (beta-1,3 linked and beta 1,6 linked glycans) which are often constituents of cells walls from pathogenic bacteria and fungi. CLEC7A is necessary for the proper inflammatory responses mediated via the TLR2 receptors and helps to mediate cytokine production in macrophages as well as their reactive oxygen response. CLEC7A also can activate T cells and stimulate their proliferation, and it is required for the engulfment of pathogenic yeast conidia. CLEC7A is a cell surface membrane receptor that operates via the SYK kinase pathways in leukocytes. CLEC7A also has multiple isoforms some of which are cytoplasmic. CLEC7A is highly expressed in leukocytes and dendritic cells and it is required for differentiation from monocytes into dendritic cell in the brain. Mutations in CLEC7A can cause an increased risk to fungal infections and in particular Candidiasis.

Immunogen

Epitope: Extracellular domain
KLH-conjugated linear peptide corresponding to the extracellular domain of Human CLEC7A/Dectin-1.

Application

Research Category
Inflammation & Immunology
Research Sub Category
Immunoglobulins & Immunology
This Anti-CLEC7A (Dectin-1) Antibody is validated for use in Western Blotting and Flow Cytometry for the detection of CLEC7A (Dectin-1).
Western Blot Analysis: A 1:1000 dilution of a representative lot of this antibody detected CLEC7A/Dectin-1 in 10 µg of Rat kidney lysate.

Flow Cytometry Analysis: 0.25 µg of a representative lot of this antibody detected CLEC7A/Dectin-1 in PBMCs and Jurkat cells.

Quality

Evaluated by Western Blotting in NIH/3T3 cell lysate.

Western Blotting Analysis: A 1:1000 dilution of this antibody detected CLEC7A/Dectin-1 in 10 µg of NIH/3T3 cell lysate.

Target description

~40 kDa observed.
This protein is highly glycosylated and may run higher than the calculated molecular weight (Ariizumi, K., et al. (2000) J. Biol. Chem. 275:20157-20167). Uncharacterized bands may be observed in some lysates.

Physical form

Antigen Affinity Purified
Purified rabbit Polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Storage and Stability

Stable for 1 year at 2-8°C from date of receipt.

Other Notes

Concentration: Please refer to lot specific datasheet.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class

10-13 - German Storage Class 10 to 13


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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