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Product Details
Synonyms
VLDLR, RP11-320E16.1, CHRMQ1, FLJ35024, VLDLRCH, VLDL receptor
Source
Human VLDL R, His Tag (VLR-H5227) is expressed from human 293 cells (HEK293). It contains AA Gly 28 - Ser 769 (Accession # P98155-2).
Predicted N-terminus: Gly 28
Request for sequenceMolecular Characterization
Other Tags and Version Biotin & Other Labeled Version
This protein carries a polyhistidine tag at the C-terminus.
The protein has a calculated MW of 84.0 kDa. The protein migrates as 90-110 kDa when calibrated against Star Ribbon Pre-stained Protein Marker under reducing (R) condition (SDS-PAGE) due to different glycosylation.
Endotoxin
Less than 0.01 EU per μg by the LAL method / rFC method.
Purity
>90% as determined by SDS-PAGE.
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.
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Performance Data
SDS-PAGE
Human VLDL R, His Tag on SDS-PAGE under reducing (R) condition. The gel was stained with Coomassie Blue. The purity of the protein is greater than 90% (With Star Ribbon Pre-stained Protein Marker).
Bioactivity-ELISA
Immobilized Human VLDL R, His Tag (Cat. No. VLR-H5227) at 5 μg/mL (100 μL/well) can bind Biotinylated Human PCSK9, Avitag,His Tag (Cat. No. PC9-H82E7) with a linear range of 10-156 ng/mL (QC tested).
Protocol
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Background
A rare neurological disorder first described in the 1970s under the name "disequilibrium syndrome" is now considered to be caused by the disruption of VLDLR gene. The disorder was renamed VLDLR-associated cerebellar hypoplasia (VLDLRCH) after a 2005 study. It is associated with parental consanguinity and found in secluded communities such as the Hutterites. VLDLRCH is one of the two known genetic disorders caused by a disruption of reelin signaling pathway, along with Norman-Roberts syndrome.
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