ALOX15 (Arachidonate 15-Lipoxygenase)
Key enzyme in lipid peroxidation and inflammation, implicated in asthma, atherosclerosis, and cancer.
Gene Information Card
| Symbol | ALOX15 |
|---|---|
| Full Name | Arachidonate 15-lipoxygenase |
| Gene Type | protein-coding |
| Chromosomal Location | 17p13.3 |
| NCBI Gene ID | 246 ncbi.nlm.nih.gov/gene/246 |
| Ensembl ID | ENSG00000161905 |
| UniProt ID | P16050 |
| OMIM ID | 152392 |
| HGNC ID | 433 |
| Aliases | 15-LOX-1, 15-LOX, 12/15-LOX, LOG15 |
Description
ALOX15 encodes arachidonate 15-lipoxygenase, an enzyme that catalyzes the peroxidation of polyunsaturated fatty acids, particularly arachidonic acid and linoleic acid, producing bioactive lipid mediators. It plays a role in inflammation, cell differentiation, and oxidative stress. The enzyme is involved in the maturation of red blood cells and the degradation of mitochondria during reticulocyte maturation. Dysregulation of ALOX15 has been linked to various diseases, including asthma, atherosclerosis, and several cancers.
Disease Associations
| Disease category | Pathophysiological mechanism | Genomic evidence |
|---|---|---|
| Asthma | Increased ALOX15 expression in airway epithelium leads to overproduction of 15-HETE, contributing to airway inflammation and remodeling. | Expression studies in human bronchial biopsies and animal models. |
| Atherosclerosis | ALOX15 oxidizes LDL, promoting foam cell formation and plaque development. | Immunohistochemistry of atherosclerotic plaques and mouse knockout models. |
| Colorectal Cancer | Altered ALOX15 expression affects apoptosis and proliferation; both tumor-suppressive and oncogenic roles reported depending on context. | Expression analysis in tumor tissues and in vitro studies. |
| Chronic Obstructive Pulmonary Disease (COPD) | Elevated ALOX15 activity contributes to oxidative stress and airway inflammation. | Gene expression studies in lung tissue from COPD patients. |
| Ischemic Stroke | ALOX15-mediated lipid peroxidation exacerbates neuronal damage after ischemia. | Animal models and human post-mortem brain analysis. |
Expression Profile
Tissue Expression
| Tissue | nTPM | level |
|---|---|---|
| Lung | 12.3 | Medium |
| Bone Marrow | 10.1 | Medium |
| Spleen | 8.5 | Low |
| Liver | 5.2 | Low |
| Blood | 4.8 | Low |
Cell Line Expression
| Cell Line | nTPM | Notes |
|---|---|---|
| A549 (Lung carcinoma) | 15.2 | High expression; used in lung cancer studies. |
| MCF7 (Breast cancer) | 8.7 | Moderate expression; linked to estrogen receptor signaling. |
| HepG2 (Liver cancer) | 6.3 | Low expression; may influence lipid metabolism. |
| THP-1 (Monocyte) | 12.0 | High expression; relevant to macrophage differentiation. |
Data source：Human Protein Atlas（proteinatlas.org）
Mutations & Variants
Hotspot Mutations
| Variant | Type | Frequency | Functional Description |
|---|---|---|---|
| c.1778C>T (p.Pro593Leu) | Missense | Rare (<0.1%) | Reduced enzyme activity in vitro; potential impact on lipid mediator production. |
| c.1565G>A (p.Arg522His) | Missense | Rare (<0.1%) | Altered substrate specificity; associated with asthma susceptibility in some populations. |
| c.−292C>T (promoter) | Regulatory | Common (MAF ~0.2) | Affects transcription factor binding; may modulate gene expression levels. |
Mutation functional classification
Loss of Function (LOF)
Loss-of-function mutations reduce or abolish 15-lipoxygenase activity, leading to decreased production of anti-inflammatory mediators and impaired resolution of inflammation.
Gain of Function (GOF)
Gain-of-function mutations increase enzyme activity, potentially enhancing lipid peroxidation and promoting oxidative stress and inflammation.
Dominant Negative (DN)
Dominant-negative mutations may interfere with dimerization or substrate binding, reducing overall enzyme activity in heterozygous individuals.
View complete mutation data：
Gene Ontology (GO)
| • arachidonate 15-lipoxygenase activity | • iron ion binding |
| • oxidoreductase activity | • lipid metabolic process |
| • inflammatory response | • cellular response to oxidative stress |
Pathways
• Arachidonic acid metabolism
• Linoleic acid metabolism
• Biosynthesis of specialized pro-resolving mediators (SPMs)
• Oxidative stress response
Protein Summary
The ALOX15 protein is a 75 kDa enzyme containing a non-heme iron center. It catalyzes the dioxygenation of polyunsaturated fatty acids, primarily arachidonic acid at carbon 15, producing 15(S)-hydroperoxyeicosatetraenoic acid (15(S)-HPETE), which is further reduced to 15(S)-HETE. It also oxygenates linoleic acid to 13(S)-HPODE. The enzyme is a monomer in solution but can form dimers. It is expressed in various tissues, including lung, bone marrow, and spleen, and is localized in the cytoplasm and nucleus. Post-translational modifications include phosphorylation, which can modulate its activity.
Related Services
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| ALOX15B Knockout HEK293 Cell Line | EDJ-KQ3377 | Human | 247 | Details Get a Quote |
| ALOX15 Knockout HEK293 Cell Line | EDJ-KQ4044 | Human | 246 | Details Get a Quote |
| ALOX15 Knockout HeLa Cell Line | EDJ-KQ52599 | Human | 246 | Details Get a Quote |
| ALOX15B Knockout HeLa Cell Line | EDJ-KQ52600 | Human | 247 | Details Get a Quote |
| ALOX15 Knockout A-549 Cell Line | EDJ-KQ61076 | Human | 246 | Details Get a Quote |
| ALOX15B Knockout A-549 Cell Line | EDJ-KQ61077 | Human | 247 | Details Get a Quote |
| ALOX15 Knockout HCT 116 Cell Line | EDJ-KQ69558 | Human | 246 | Details Get a Quote |
| ALOX15B Knockout HCT 116 Cell Line | EDJ-KQ69559 | Human | 247 | Details Get a Quote |
| ALOX15（p.R205Q） Point Mutation in A-549 Cell Line | EDC03241 | Human | 246 | Details Get a Quote |
| ALOX15（p.T560M） Point Mutation in A-549 Cell Line | EDC03217 | Human | 240 | Details Get a Quote |
| ALOX15（p.N103K） Point Mutation in A-549 Cell Line | EDC03253 | Human | 246 | Details Get a Quote |
| ALOX15（p.P617S） Point Mutation in A-549 Cell Line | EDC03250 | Human | 246 | Details Get a Quote |
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