Human CLEC5A / MDL-1 Protein, His Tag, active dimer, low endotoxin (MALS & SPR verified)

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CLA-H5243-100ug
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CLA-H5243-1mg (500ug X 2)
$3,170.00
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CLA-H5243
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Synonyms

CLEC5A, CLECSF5, superfamilymember 5, C-type lectin domain family 5, member A, MDL1, MDL-1, DAP12-associating lectin 1

Source

Human CLEC5A, His Tag (CLA-H5243) is expressed from human 293 cells (HEK293). It contains AA Pro 28 - Lys 188 (Accession # Q9NY25-1).

Predicted N-terminus: His

Molecular Characterization

This protein carries a polyhistidine tag at the N-terminus.

The protein has a calculated MW of 39.0 kDa. The protein migrates as 60-66 kDa when calibrated against Star Ribbon Pre-stained Protein Marker under reducing (R) condition (SDS-PAGE) due to glycosylation.

Endotoxin

Less than 0.01 EU per μg by the LAL method / rFC method.

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.

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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

CLEC5A, also known as MDL1 and MDL-1, is a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily.CLEC5A is expressed on monocytes, macrophages, and neutrophils. Its expression is up-regulated on monocytes in rheumatoid arthritis. CLEC5A with dnax-activation protein 12 and may play a role in cell activation. It also functions as a positive regulator of osteoclastogenesis. CLEC5A acts as a key regulator of synovial injury and bone erosion during autoimmune joint inflammation .The binding of dengue virus to CLEC5A triggers signaling through the phosphylation of TYROBP, this interaction does not result in viral entry, but stimulates proinflammatory cytokine release.