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.

Human,Mouse,Rat,Dog,Pig,Cow

IHC,IF,ICC

IHC 1:100-500
IF 1:100-500
ICC 1:100-1:400

176kD

4041

O75197

https://www.uniprot.org/uniprotkb/O75197

Membrane; Single-pass type I membrane protein. Endoplasmic reticulum (By similarity). Note=Chaperoned to the plasma membrane by MESD (By similarity).

Widely expressed, with the highest level of expression in the liver and in aorta.

KLH conjugated Synthesised phosphopeptide derived from human LRP5 around the phosphorylation site of Thr1492

Rabbit

Polyclonal

IgG

affinity purified by Protein A

Liquid

0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.

Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.