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- SPECIES: Human
- SOURCE SPECIES: HEK293 cells
- RECOMBINANT PROTEIN SEQUENCE: Gly 28 - Ser 797
- FUSION TAG: His Tag
- TESTED APPLICATIONS: WB
- APPLICATION NOTE: This recombinant protein can be used for WB. For research use only.
- PREDICTED MOLECULAR WEIGHT: 83 kDa, The protein migrates as 110-120 kDa under reducing (R) condition (SDS-Page) due to different glycosylation.
- BIOLOGICAL ACTIVITY: Measured by its binding ability in a functional ELISA. When Recombinant Human Apolipoprotein E3 is immobilized at 1μg/ml (100μl/well), the concentration of Recombinant Human VLDLR that produces 50% of the optimal binding response is found to be approximately 0. 03 - 0. 15μg/ml.
Properties
- PURITY: >97% as determined by SDS-PAGE.
- PHYSICAL STATE: Lyophilized
- BUFFER: PBS, pH7.4
- STORAGE CONDITIONS: Lyophilized Protein should be stored at -20°C or lower for long term storage. Upon reconstitution, working aliquots should be stored at -20°C or -70°C. Avoid repeated freeze-thaw cycles.
Additional Info
- NCBI OFFICIAL SYMBOL: VLDLR
- ADDITIONAL NAMES: VLDLR, RP11-320E16.1, CHRMQ1, FLJ35024, VLDLRCH, VLDL receptor
- Protein Accession Number: AAI42654
- NCBI GENE ID NUMBER: 7436
Background
- The very-low-density-lipoprotein receptor (VLDL-R) is a lipoprotein receptor that shows considerable similarity to the lowdensity-lipoprotein receptor. VLDL R is a 130 kDa type I transmembrane protein in the LDL receptor family that plays a significant role in lipid metabolism and in nervous system development and function .This receptor has been suggested to be important for the metabolism of apoprotein-E-containing triacylglycerol-rich lipoproteins, such as very-low-densitylipoprotein (VLDL), beta-migrating VLDL and intermediate-density lipoprotein. It is also one of the receptors of reelin, an extracellular matrix protein which regulates the processes of neuronal migration and synaptic plasticity. In humans, the VLDL-R is encoded by the VLDLR gene.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.
- 1: Sakai J, Hoshino A, Takahashi S, et al., 269 (3): 2173–82.
- 2: Moheb LA, Tzschach A, Garshasbi M, et al. Eur. J. Hum. Genet. 16 (2): 270–3.
- 3: Boycott KM, Flavelle S, Bureau A, et al., 2005, Am. J. Hum. Genet. 77 (3): 477–83.
Disclaimer
- FOR RESEARCH USE ONLY
For additional information, visit ProSci's Terms & Conditions Page. - Disclaimer: Products are intended for laboratory research purposes only and should be used by qualified personnel only. They are not intended for use in humans. ProSci is not liable for damages or injuries resulting from receipt and/or use of ProSci materials. Please refer to the Material Safety Data Sheet (MSDS) for safe storage, handling, and use procedures.
Shipping Info
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