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Kevin Eric Smith
What is TAK1 and why is it important to inhibit its potentially destructive pathway?
Gout, Inflammation and Joint Pain Control
TAK1 is an enzyme and signaling molecule in humans encoded by the MAP3K7 gene (a mitogen-activated protein). TAK1 regulates cellular death through various pathways. As we have discussed before, programmed cell death is a normal, physiologic process intended to help remove damaged cells. However, unattended cell death is the direct pathway for human disease. TAK1 contains binding proteins that are responsible for cell viability and tissue balance in a variety of organs.
TAK1 is a key molecular component that can readily determine of the fate of our body's cells. TAK1 has been typically considered pro-survival, however, recent studies have determined that various factors could cause it to induce cell death. Scientifically speaking, studies are exploring the ability to inhibit TAK1 as a therapeutic approach to killing off rogue cancer cells and stopping chronic inflammatory response.
Researchers at Washington State University Health Sciences Spokane and others have recently conducted studies involving the treatment of Gout by suppressing the inflammation via the inhibition of TAK1. Uric acid crystals that are formed and accumulate in the joints are perceived as an attack on the human body and naturally triggers an immune system response. The cytokine protein, IL-1-beta, is released to help "fight off the attack" and the inflammation ensues as a result.
"It's kind of a vicious cycle that starts with these crystals, which cause IL-1-beta to be produced, inducing inflammation and activating a lot of other proteins to produce more inflammation," said Salah-Uddin Ahmed, a professor of pharmaceutical sciences in the WSU College of Pharmacy and Pharmaceutical Sciences and senior author on the study.
One of the proteins that are activated by IL-1-beta is TAK1. The research team found that uric acid crystals
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