Ubiquitin Ligase Smurf1 Functions in Selective Autophagy of Mycobacterium tuberculosis & Anti-TB Host Defense

University of Texas (UT) Southwestern Medical Center researchers have identified a protein that is central to the immune system’s ability to recognize and destroy the bacterium responsible for the global tuberculosis (TB) epidemic. The new finding, reported in the January 11, 2017 issue of Cell Host & Microbe, could someday lead to the development of immunity-based therapies to treat tuberculosis – which typically takes months to eradicate and has become increasingly resistant to antibiotics – by strengthening this immune pathway, said Dr. Michael Shiloh, Assistant Professor of Internal Medicine and Microbiology. The article is titled “The Ubiquitin Ligase Smurf1 Functions in Selective Autophagy of Mycobacterium tuberculosis and Anti-Tuberculous Host Defense.” According to the World Health Organization, TB is a top infectious disease killer worldwide and is estimated to have infected 9.5 million people and caused 1.5 million deaths in 2014. That year, tuberculosis surpassed HIV as the world’s most lethal infection. “The protein Smurf1 functions in specialized white blood cells called macrophages in both mice and humans, thereby suggesting a conserved evolutionary pathway,” said Dr. Shiloh, co-senior author of the study along with Dr. Beth Levine, Director of the University’s Center for Autophagy Research. In 2011, UT Southwestern researchers in Dr. Levine’s laboratory identified the protein Smurf1 as important for the elimination of viruses and damaged mitochondria from cells via a cellular housekeeping process called autophagy. Dr. Levine is also a Professor of Internal Medicine and Microbiology; a Howard Hughes Medical Institute Investigator; and holder of the Charles Cameron Sprague Distinguished Chair in Biomedical Science.
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