Recombinant Human LRP-5 GST (N-Term) Protein Summary
Description |
A recombinant protein with a N-terminal GST tag corresponding to the amino acid sequence 41-130 of Human LRP-5 Source: Wheat Germ (in vitro) Amino Acid Sequence: RDVRLVDAGGVKLESTIVVSGLEDAAAVDFQFSKGAVYWTDVSEEAIKQTYLNQTGAAVQNVVISGLVSPDGLACDWVGKKLYWTDSETN |
Preparation Method |
in vitro wheat germ expression system |
Details of Functionality |
This protein was produced in an in vitro wheat germ expression system that should preserve correct conformational folding that is necessary for biological function. While it is possible that this protein could display some level of activity, the functionality of this protein has not been explicitly measured or validated. |
Source |
Wheat germ |
Protein/Peptide Type |
Recombinant Protein |
Gene |
LRP5 |
Purity |
>80% by SDS-PAGE and Coomassie blue staining |
Applications/Dilutions
Dilutions |
- ELISA
- Immunoaffinity Purification
- Protein Array
- Western Blot
|
Theoretical MW |
35.64 kDa. Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors. |
Packaging, Storage & Formulations
Storage |
Store at -80C. Avoid freeze-thaw cycles. |
Buffer |
50 mM Tris-HCI, 10 mM reduced Glutathione, pH 8.0 in the elution buffer. |
Preservative |
No Preservative |
Purity |
>80% by SDS-PAGE and Coomassie blue staining |
Notes
This product is produced by and distributed for Abnova, a company based in Taiwan.
Alternate Names for Recombinant Human LRP-5 GST (N-Term) Protein
Background
LRP5 is involved in the Wnt/beta catenin signaling pathway, probably by acting as a coreceptor together with Frizzled for Wnt. Defects in LRP5 are a cause of autosomal dominant and autosomal recessive familial exudative vitreoretinopathy (FEVR). Autosomal dominant FEVR is also referred to as exudative vitreoretinopathy 1 (EVR1); also known as Criswick-Schepens syndrome. FEVR is a disorder of the retinal vasculature characterized by an abrupt cessation of growth of peripheral capillaries, leading to an avascular peripheral retina. This may lead to compensatory retinal neovascularization, which is thought to be induced by hypoxia from the initial avascular insult. New vessels are prone to leakage and rupture causing exudates and bleeding, followed by scarring, retinal detachment and blindness. FEVR is reported to have a penetrance of 100%, but clinical features can be highly variable, even within the same family. Patients with mild forms of the disease are asymptomatic, and their only disease-related abnormality is an arc of avascular retina in the extreme temporal periphery.
Limitations
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Peptides and proteins are
guaranteed for 3 months from date of receipt.
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