Researchers at the University of Pennsylvania School of Medicine recently identified how a
regulatory protein called Bcl-3 helps to control the body’s
inflammation response to infection by interfering a critical biochemical process called ubiquitination*.
Without Bcl-3, Chen says
p50 cannot stop the inflammation response, but instead will become degraded very fast, through ubiquintination. During exposure to infection, Bcl-3 appears to overrule the p50 ubiquitination, stabilizing the presence of p50 on DNA and halting inflammation. “Bcl-3 appears to take in information from the body and, in response to infection, interferes with p50 degradation to decrease
inflammatory response.Bcl-3 thus helps regulate inflammation”
“By mimicking Bcl-3 activity, we hope to create new ways to control inflammation for therapeutic purposes with selective anti-inflammatory agents” In the laboratory of senior author Youhai Chen, PhD, Associate Professor of Pathology and Laboratory Medicine, Carmody and others searched for clues as to how Bcl-3 controls inflammation by examining how Bcl-3-deficient mouse cells respond to infection.
“Since Bcl-3 acts on specific genes, we should be able to target a subset of dangerous regulatory genes without disrupting other important immune responses.” Such drugs could benefit patients with chronic inflammation and transplant recipients as well as those suffering with inflammatory diseases.
*Ubiquitination is an intracellular system of checks and balances, where cellular proteins are flagged for disposal.check out the link for further details.
More abstracts about the finding of a key protein that stops inflammation