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Recombinant Human CLEC3B protein (mFc Tag) (HPLC verified)

Species

Human

Purity

>90 %, SDS-PAGE
>90 %, SEC-HPLC

Tag

mFc Tag

Activity

not tested

Cat no : Eg3608

Validation Data Gallery

  • Purity of Recombinant Human CLEC3B was determined by SDS-PAGE. The protein was resolved in an SDS-PAGE in reducing (R) and non-reducing (NR) conditions and stained using Coomassie blue.

    Purity of Recombinant Human CLEC3B was determined by SDS-PAGE. The protein was resolved in an SDS-PAGE in reducing (R) and non-reducing (NR) conditions and stained using Coomassie blue.

  • The purity of Human CLEC3B was greater than 90% as determined by SEC-HPLC.

    The purity of Human CLEC3B was greater than 90% as determined by SEC-HPLC.

Product Information

Purity >90 %, SDS-PAGE
>90 %, SEC-HPLC
Endotoxin <0.1 EU/μg protein, LAL method
Activity 
Not tested
Expression HEK293-derived Human CLEC3B protein Glu22-Vla202 (Accession# P05452) with a mouse IgG Fc tag at the C-terminus.
GeneID 7123
Accession P05452
PredictedSize 46.8 kDa
SDS-PAGE 44-50 kDa, reducing (R) conditions
Formulation Lyophilized from 0.22 μm filtered solution in PBS, pH 7.4. Normally 5% trehalose and 5% mannitol are added as protectants before lyophilization.
Reconstitution Briefly centrifuge the tube before opening. Reconstitute at 0.1-0.5 mg/mL in sterile water.
Storage Conditions
It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
  • Until expiry date, -20℃ to -80℃ as lyophilized proteins.
  • 3 months, -20℃ to -80℃ under sterile conditions after reconstitution.
Shipping The product is shipped at ambient temperature. Upon receipt, store it immediately at the recommended temperature.

Background

C-Type Lectin Domain Family 3 Member B (CLEC3B) is a transmembrane Ca2+-binding protein, located in cell plasma, extracellular matrix, and exosomes. CLEC3B functions in the mineralization process in osteogenesis and neuroprotection and is associated with tumor invasion and metastasis via plasminogen activation, leading to extracellular proteolysis. Downregulation of CLEC3B has been reported in various diseases such as hepatocellular carcinoma, ovarian cancer, oral squamous cell carcinoma, and many other cancers. It was demonstrated in CLEC3B-deficient mice that the absence of CLEC3B impeded the mineralization process in osteogenesis.

References:

1.Dai W. et al. (2019). Cell Commun Signal. 17(1):113. 
2.Xie XW. et al. (2021). Front Mol Biosci. 7:614034.
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