Biotinylated Human BLAME / SLAMF8 Protein, His,Avitag™

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BLE-H82E4-25ug
$360.00
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BLE-H82E4-200ug
$1,565.00
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BLE-H82E4
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Synonyms

BLAME, SLAMF8, CD353

Source

Biotinylated Human BLAME, His,Avitag (BLE-H82E4) is expressed from human 293 cells (HEK293). It contains AA Ala 23 - Asp 233 (Accession # Q9P0V8-1).

Molecular Characterization

This protein carries a polyhistidine tag at the C-terminus, followed by an Avi tag (Avitag™).

The protein has a calculated MW of 27.1 kDa. The protein migrates as 30-35 kDa 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

>85% as determined by SDS-PAGE.

Formulation

Lyophilized from 0.22 μm filtered solution in 50 mM Sodium Citrate, 150 mM NaCl, pH5.5 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.

배경 소개

BLAME (B-lymphocyte activator macrophage expressed) is also known as SLAM family member 8(SLAMF8), CD353. BLAME is a cell surface receptor that is expressed upon activation of macrophages (MΦs) by IFN-γ or bacteria, is a negative regulator of ROS in response to Gram+ and Gram- bacteria. May play a role in B-lineage commitment and/or modulation of signaling through the B-cell receptor. SLAMF8 is a costimulatory molecule that affects the activation of macrophages in inflammation and in immunosuppression and inflammation response to glioma cells could aid immunotherapy for glioma.