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FHL3
SNP Table
| variant | genotype | frequency | risk allele |
|---|---|---|---|
| rs7366048 | |||
| rs142528167 | |||
| rs149245838 | |||
| rs192670727 | |||
| rs11211085 | |||
| rs12724533 | |||
| rs4274021 | |||
| rs4634868 | |||
| rs57918347 | |||
| rs111681950 | |||
| rs1136994 | |||
| rs11485996 | |||
| rs11488567 | |||
| rs12729989 | |||
| rs28411034 | |||
| rs41310438 | |||
| rs61778084 | |||
| rs61778086 | |||
| rs9660548 | |||
| rs114296424 |
Find on This Page
Summary
The FHL3 gene may be involved in the COX-2-mediated formation of prostaglandins, hormone-like substances that have been linked to inflammation and pain. Variants of FHL3 may play a role in rheumatoid arthritis by increasing the production of COX-2.
Lifestyle, diet, and supplement modifications may counteract the effects of these variants by lowering COX-2 production and/or activity.
Protein names
Found in These Blog Articles
More Information
FHL3 is a protein that activates the gene regulator CREB [R].
In the brain, CREB plays essential roles in mediating memory formation and consolidation. In the most mobile and common type of joint in the human body (the synovial joint), CREB may promote the formation of prostaglandin E2 by increasing production of the COX-2 enzyme [R, R].
Prostaglandins are hormone-like substances with many functions, including the ability to promote inflammation and pain in synovial joints. In this manner, prostaglandins may contribute to the progression of the autoimmune disorder rheumatoid arthritis [R].
Variants of FHL3 have been associated with rheumatoid arthritis. These variants may increase the production of FHL3, leading to the CREB-mediated activation of COX-2 and excess prostaglandin E2 formation [R, R, R, R, R].
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