Biotinylated Human CLEC12A / MICL / CLL-1 Protein, Fc,Avitag™ (MALS verified)

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CLA-H82F7-25ug
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CLA-H82F7-200ug
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CLA-H82F7
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Synonyms

CLEC12A, MICL, CLL-1, CLL1, DCAL2, DCAL-2, CD371

Source

Biotinylated Human CLEC12A, Fc,Avitag (CLA-H82F7) is expressed from human 293 cells (HEK293). It contains AA His 65 - Ala 265 (Accession # Q5QGZ9-2).

Predicted N-terminus: Gly

Molecular Characterization

This protein carries an Avi tag (Avitag™) at the N-terminus, followed by a human IgG1 Fc tag.

The protein has a calculated MW of 51.9 kDa. The protein migrates as 65-80 kDa when calibrated against Star Ribbon Pre-stained Protein Marker under reducing (R) condition (SDS-PAGE) due to glycosylation.

Labeling

Biotinylation of this product is performed using Avitag™ technology. Briefly, the single lysine residue in the Avitag is enzymatically labeled with biotin.

Protein Ratio

Passed as determined by the SABA assay / HABA assay / binding ELISA.

Purity

>95% as determined by SDS-PAGE.

>95% as determined by SEC-MALS.

Formulation

Lyophilized from 0.22 μm filtered solution in PBS, pH7.4 with trehalose as protectant.

Contact us for customized product form or formulation.

Reconstitution

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

Shipping and Storage

This product is shipped at ambient temperature.

For long term storage, the product should be stored at lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:
  • -20°C to -70°C for 12 months in lyophilized state;
  • -70°C for 3 months under sterile conditions after reconstitution.

Background

CLEC12A (C-type lectin domain family 12 member A) is also known as CLL1, DCAL2, MICL. Clec12a is an inhibitory receptor for uric acid crystals that regulates inflammation in response to cell death. Cell surface receptor that modulates signaling cascades and mediates tyrosine phosphorylation of target MAP kinases. Evidence of distinct disease propagating stem cells in myelodysplastic syndrome (MDS) has emerged in recent years. The role of CLEC12A in MDS, however, remains to be elucidated. Furthermore, CLEC12A has been proposed as a promising marker of leukaemic stem cells in AML.