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Recombinant human LDLR Protein, His Tag, 100µg  

Recombinant human LDLR Protein, His Tag, 100µg

Recombinant Human LDLR /LDL Receptor Protein (rhLDLR) Ala 22-Arg788 was produced in human 293 cells (HEK293), His tag

Synonyms: recombinant human protein, LDLR, FH, FHC, LDLCQ2, Low-Density Lipoprotein (LDL) Receptor, LDL receptor protein

More details

LDR-H5224-100

Availability: within 7 days

420,00 €

Background: Low-Density Lipoprotein (LDL) Receptor, also known as LDLR, FH, FHC, LDLCQ2, and is a mosaic protein of ~840 amino acids (after removal of signal peptide) that mediates the endocytosis of cholesterol-rich LDL. It is a cell-surface receptor that recognizes the apoprotein B100 which is embedded in the phospholipid outer layer of LDL particles. The receptor also recognizes the apoE protein found in chylomicron remnants and VLDL remnants (IDL). [1] It belongs to the Low density lipoprotein receptor gene family.[2] LDL receptor complexes are present in clathrin-coated pits (or buds) on the cell surface, which when bound to LDL-cholesterol via adaptin, are pinched off to form clathrin-coated vesicles inside the cell. This allows LDL-cholesterol to be bound and internalized in a process known as endocytosis and prevents the LDL just diffusing around the membrane surface. This occurs in all nucleated cells (not erythrocytes), but mainly in the liver which removes ~70% of LDL from the circulation. Synthesis of receptors in the cell is regulated by the level of free intracellular cholesterol; if it is in excess for the needs of the cell then the transcription of the receptor gene will be inhibited. LDL receptors are translated by ribosomes on the endoplasmic reticulum and are modified by the Golgi apparatus before travelling in vesicles to the cell surface. LDL is directly involved in the development of atherosclerosis, due to accumulation of LDL-cholesterol in the blood. Atherosclerosis is the process responsible for the majority of cardiovascular diseases.[3-4]

Source
Recombinant Human LDLR /LDL Receptor Protein (rhLDLR) Ala 22-Arg788 (Accession # NP_000518.1 ) was produced in human 293 cells (HEK293)

Molecular Characterization
rhLDLR, fused with a C-terminal 6×his tag and has a calculated MW of 86 kDa. The predicted N-terminal is Ala22 or Asp193. Corresponding to the mature and immature form, DTT-reduced protein migrates as 95-110 kDa &125-140 kDa polypeptide in SDS-PAGE resulting from different glycosylation.

Endotoxin
Less than 1.0 EU per μg of the rhLDLR by the LAL method.

Purity
>90% as determined by SDS-PAGE.

Formulation
Lyophilized from 0.22 μm filtered solution in PBS, pH 7.4. Normally Mannitol or Trehalose are added as protectants before lyophilization.

Reconstitution
See Certificate of Analysis for details of reconstitution instruction and specific concentration.

Storage
Avoid repeated freeze-thaw cycles.
No activity loss was observed after storage at:
In lyophilized state for 1 year (4C-8C); After reconstitution under sterile conditions for 1 month (4C-8C) or 3 months (-20C to -70C). 

Bioactivity:
(1) Measured by its binding ability in a functional ELISA.
Immobilized Human LDL R, His Tag (Cat# LDR-H5224) at 10 μg/mL (100 μl/well) can bind Biotinylated Human PCSK9 (Cat# PC9-H82E7 ) with a linear range of 0.01-0.1 μg/mL.
(2) Measured by its binding ability in a functional ELISA.
Immobilized Human LDL R, His Tag (Cat# LDR-H5224) at 10 μg/mL (100 μl/well) can bind Biotinylated Human (D374Y) PCSK9 (Cat# PCY-H82E7 ) with a linear range of 0.02-0.5 μg/mL.

References

(1) Yamamoto T, et al., 1984, Cell 39 (1): 27–38.
(2) Nykjaer A, Willnow TE, 2002, Trends Cell Biol. 12 (6): 273–80.
(3) Barrett P.H., Watts G.F. 2002, Atherosclerosis. Supplements. 2: 1-4.
(4) Nomura S. et al., 2004, Gene. Therapy. 11: 1540-1548.