CLEC12A/CLL-1 (E5T5V) Rabbit mAb #57950
- WB
- IP
- F
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 55-75 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:100 |
| Flow Cytometry (Live) | 1:200 - 1:800 |
Storage
Protocol
Specificity / Sensitivity
CLEC12A/CLL-1 (E5T5V) Rabbit mAb recognizes endogenous levels of total CLEC12A/CLL-1 protein.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human CLEC12A/CLL-1 protein.
Background
Part of the NK gene complex, C-type lectin-like molecule 1 (MICL/DCAL-2/CLL-1/CLEC12A) encodes a type-II transmembrane glycoprotein whose expression is largely restricted to hematopoietic cells of the myeloid lineage such as monocytes, macrophages, dendritic cells, and neutrophils (1-3). Research studies have shown that CLL-1 possesses a single C-type lectin-like domain within the extracellular domain and a single ITIM motif within its short cytoplasmic tail, which facilitates association with inhibitory SH2 domain-containing tyrosine phosphatases, SHP-1 and SHP-2. It is thought that signaling through the ITIM motif of CLL-1 facilitates inhibition of myeloid cell activation (1,2). By serving as a receptor for DAMPs that become exposed on dead cells, such as uric acid crystals, CLL-1 restrains pro-inflammatory immune responses that occur in response to cell death (4). In addition to being expressed on normal differentiated myeloid cells, research studies have also demonstrated expression of CLL-1 on the surface of malignant myeloid cells (5). As a result, CLL-1 has received significant attention as a potential novel therapeutic target for AML as its expression is absent from normal hematopoietic stem cells but is highly overexpressed on AML stem cells (5-9).
- Marshall, A.S. et al. (2004) J Biol Chem 279, 14792-802.
- Marshall, A.S. et al. (2006) Eur J Immunol 36, 2159-69.
- Chen, C.H. et al. (2006) Blood 107, 1459-67.
- Neumann, K. et al. (2014) Immunity 40, 389-99.
- Bakker, A.B. et al. (2004) Cancer Res 64, 8443-50.
- Jiang, Y.P. et al. (2018) Blood Adv 2, 1738-49.
- Tashiro, H. et al. (2017) Mol Ther 25, 2202-13.
- Wang, J. et al. (2018) J Hematol Oncol 11, 7.
- Laborda, E. et al. (2017) Int J Mol Sci 18.
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