OLR1

(redirected from LOX-1)

OLR1

A gene on chromosome 12p13.2-p12.3 that encodes a C-type lectin domain receptor which mediates the recognition, internalisation and degradation of oxidatively modified low-density lipoprotein (oxLDL) by vascular endothelial cells. It is also a receptor for advanced glycation end (AGE) products, activated platelets, monocytes, apoptotic cells and both Gram-negative and Gram-positive bacteria, as well as for HSP70 protein, which is involved in antigen cross-presentation to naïve T-cells. OLR1 is also involved in inflammation, acting as a leukocyte-adhesion molecule at the vascular interface in endotoxin-induced inflammation.
References in periodicals archive ?
Keywords: Ginkgo biloba Atherosclerosis Activated platelets ROS LOX-1 p38MAPK Isobole
Aim: In the present study, we investigated whether the therapeutic dosages of Ginkgo biloba extract (EGb) and Aspirin (ASP) might synergistically suppress oxidative stress through regulating the expressions of LOX-1 and phosphorylatal p38MAPK (p-p38MAPK) in human coronary artery endothelial cells (HCAECs) ex vivo.
extend their studies of CRP and LOX-1 in 2 important ways.
A more detailed structural study is required to formally verify the manner by which CRP and LOX-1 interact.
Aortic LOX-1 (lectin-like oxidized low-density lipoprotein receptor-1) mRNA and protein increased after ozone exposure, and LOX-1 protein increased after exposure to ozone + DEP.
We conclude that there is a possible role of oxidized lipids and protein through LOX-1 and/or RAGE signaling.
Recently, we showed that CRP bound to CHO cells (hLOX-1-CHO) expressing human lectin-like oxidized LDL receptor 1 (LOX-1), and that CRP bound to recombinant human LOX-1 in a cell-free system (19, 20).
The CHO cell line hLOX-1-CHO, which expresses human LOX-1 in a tetracycline-inducible manner, was maintained with Ham's F12, 10% fetal bovine serum, and 1% antibiotics-antimycotics (Invitrogen) as described (19).
Mice lacking LOX-1 are protected against atherosclerosis, whereas transgenic LOX-1 overexpression increases atherosclerotic lesion size.
Activation of LOX-1 in endothelial cells induces various changes relevant to endothelial dysfunction, e.
Members of the scavenger receptor family, such as class A scavenger receptor (SR-A), CD36, LOX-1, and scavenger receptor B-I (SR-BI), recognize common ligands such as modified LDL, bacteria, and advanced glycation end products, and they are thought to affect the progression of atherosclerosis (11, 12).
LOX-1 expressed on the cell surface is proteolytically cleaved at its membraneproximal extracellular domain (ECD) and released in soluble form (sLOX-1) (2,3).