OLR1 Human, HEK

The OLR1 gene is located on chromosome 12 (12p13.2) in humans . The gene is regulated through the cyclic AMP signaling pathway and can produce multiple transcript variants through alternative splicing . The protein itself is a type II membrane protein with a C-type lectin-like domain, which is responsible for binding oxLDL .

LOX-1 is primarily expressed on endothelial cells, macrophages, and smooth muscle cells . Under normal conditions, the expression of LOX-1 on endothelial cells is relatively low. However, it can be significantly upregulated by various atherosclerotic stimuli such as tumor necrosis factor-alpha (TNF-α), oxLDL, and blood vessel shear stress .

The primary function of LOX-1 is to bind, internalize, and degrade oxLDL . OxLDL is a marker of atherosclerosis and induces vascular endothelial cell activation and dysfunction, leading to pro-inflammatory responses, oxidative stress, and apoptosis . LOX-1 also plays a role in the regulation of Fas-induced apoptosis .

Mutations and dysregulation of the OLR1 gene have been associated with several cardiovascular diseases, including atherosclerosis and myocardial infarction . The receptor’s role in endothelial dysfunction and plaque formation makes it a critical target for understanding and potentially treating these conditions .

Additionally, LOX-1 has been implicated in other pathological processes, such as Alzheimer’s disease, due to its involvement in oxidative stress and inflammation .

Human recombinant LOX-1, produced in HEK (Human Embryonic Kidney) cells, is widely used in research to study its structure, function, and role in disease. This recombinant protein allows for detailed biochemical and biophysical analyses, facilitating the development of therapeutic strategies targeting LOX-1 .