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OLR1

Protein-coding gene in the species Homo sapiens From Wikipedia, the free encyclopedia

Oxidized low-density lipoprotein receptor 1 (Ox-LDL receptor 1) also known as lectin-type oxidized LDL receptor 1 (LOX-1) is a protein that in humans is encoded by the OLR1 gene.[5]

AliasesOLR1, CLEC8A, LOX1, LOXIN, SCARE1, SLOX1, oxidized low density lipoprotein receptor 1
External IDsOMIM: 602601; MGI: 1261434; GeneCards: OLR1
PDBOrtholog search: PDBe RCSB
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OLR1
Identifiers
AliasesOLR1, CLEC8A, LOX1, LOXIN, SCARE1, SLOX1, oxidized low density lipoprotein receptor 1
External IDsOMIM: 602601; MGI: 1261434; GeneCards: OLR1
Available structures
PDBOrtholog search: PDBe RCSB
Orthologs
DatabasesNCBI: entry; OMA: entry
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001172632
NM_001172633
NM_002543

NM_001301094
NM_001301096
NM_138648

RefSeq (protein)

NP_001166103
NP_001166104
NP_002534

NP_001288023
NP_001288025
NP_619589

Location (UCSC)Chr 12: 10.16 – 10.17 MbChr 6: 129.46 – 129.48 Mb
PubMed search[3][4]
Wikidata
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LOX-1 is the main receptor for oxidized LDL on endothelial cells, macrophages, smooth muscle cells,[6] and other cell types.[7] But minimally oxidized LDL is more readily recognized by the TLR4 receptor, and highly oxidized LDL is more readily recognized by the CD36 receptor.[8]

Function

LOX-1 is a receptor protein which belongs to the C-type lectin superfamily. Its gene is regulated through the cyclic AMP signaling pathway. The protein binds, internalizes and degrades oxidized low-density lipoprotein.[citation needed]

Normally, LOX-1 expression on endothelial cells is low, but tumor necrosis factor alpha, oxidized LDL, blood vessel shear stress, and other atherosclerotic stimuli substantially increase LOX-1 expression.[7][9]

LOX-1 may be involved in the regulation of Fas-induced apoptosis. Oxidized LDL induces endothelial cell apoptosis through LOX-1 binding.[6] Other ligands for LOX-1 include oxidized high-density lipoprotein, advanced glycation end-products, platelets, and apoptotic cells.[6][9] The binding of platelets to LOX-1 causes a release of vasoconstrictive endothelin, which induces endothelial dysfunction.[9]

Clinical significance

Binding of oxidized LDL to LOX-1 activates NF-κB, leading to monocyte adhesion to enthothelial cells (a pre-requisite for the macrophage foam cell formation of atherosclerosis).[7] Macrophage affinity for unmodified LDL particles is low, but is greatly increased when the LDL particles are oxidized.[10] LDL oxidation occurs in the sub-endothelial space, rather than in the circulation.[10] But oxidized cholesterol from foods cooked at high temperature can also be a source of oxysterols.[8]

OLR1 gene polymorphisms have been associated with coronary artery disease.[11]

References

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