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Recycling of 'chauffeur protein' helps regulate fat production
Date:2/10/2014

Studying a cycle of protein interactions needed to make fat, Johns Hopkins researchers say they have discovered a biological switch that regulates a protein that causes fatty liver disease in mice. Their findings, they report, may help develop drugs to decrease excessive fat production and its associated conditions in people, including fatty liver disease and diabetes.

A summary of the research appeared online on Jan. 29 in the Journal of Biological Chemistry.

"We've learned how the body finely tunes levels of a protein called SCAP that is required to turn on fat production in cells," says Peter Espenshade, Ph.D., professor of cell biology at the Johns Hopkins University School of Medicine. "We hope this new information will eventually lead to interventions that could help people suffering from obesity-induced fatty liver disease and diabetes."

Espenshade explains that fats, which include cholesterol, are essential to the life of organisms, but too much can sabotage systems that rid the body of toxins and regulate hormones, among other functions. Crucial to the right balance of fats is a family of proteins called sterol regulatory element-binding proteins (SREBPs), which turn on fat-making genes when fat levels in cells are low.

SREBPs are made and embedded in the membrane of the cellular compartment called the endoplasmic reticulum, or ER. To get to the cell's nucleus to turn on genes, the business end of SREBPs has to be clipped away from the membrane. Two different proteins, S1P and S2P, make those clips in sequence. But S1P and S2P live in a different cellular compartment, known as the Golgi.

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Contact: Catherine Kolf
ckolf@jhmi.edu
443-287-2251
Johns Hopkins Medicine
Source:Eurekalert

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