Averil Ma, MD
|Title||Professor in Residence|
|School||UCSF School of Medicine|
|Address||513 Parnassus Ave, Med Sci|
San Francisco CA 94143
|2010||Chief, UCSF Division of Gastroenterology|
||2012||Chair, NIH CMI-A study section|
|2001||AGA/GRG Young Investigator Award|
|1997||Cancer Research Institute Scholar|
|1989||James McDonnell Scholar|
Dr. Ma is Chief of the Division of Gastrenterology and Hepatology at the UCSF Parnassus and Mt Zion sites and Director of the UCSF Colitis and Crohn's Disease Center. His laboratory studies factors that regulate inflammation. The laboratory discovered the critical role of A20, a ubiquitin modifying enzyme, in preventing inflammation (Lee et al, Science). They found that A20 restricts basal Myd88 dependent signals to prevent this inflammation (Boone et al, Nat Immunol; Turer et al, J Exp Med).
Biochemically, they have discovered that A20 is a de-ubiquitinating enzyme (Boone et al, Nature Immunology) that also exhibits E3 ligase activity (Wertz et al, Nature). In addition, non-catalytic mechanisms may contribute to A20’s biochemical functions (Skaug et al, Mol Cell). Another important component of A20-mediated regulation of signaling may be ABIN-1, a protein that binds to A20. By generating ABIN-1 deficient mice, they discovered that ABIN-1, like A20, restricts TNF induced cell death and preserves embryonic survival (Oshima et al, Nature). While A20 is a ubiquitin editing enzyme, ABIN-1 is a ubiquitin sensor with no known enzymatic activity.
The lab has generated mice lacking A20 in selected lineages and shown that A20 deficiency in B cells causes SLE-like disease (Tavares et al, Immunity). By contrast, mice lacking A20 in dendritic cells develop colitis, sero-negative arthritis and spondyloarthritis (Hammer et al, Nature Immunology). Hence, these mice resemble a stereotypical syndrome resembling human patients with IBD and sero-negative arthritis. They are now using these mice and cells to investigate the links between ubiquitin dependent intracellular signaling and inflammatory/autoimmune diseases such as IBD.
A20 and ABIN-1 mutations are linked to human lymphomas, rheumatoid arthritis, SLE, psoriasis, sprue and IBD (Musone et al, Nature Genetics). Given the strong genetic links between these ubiquitin modifying enzymes and human diseases, the group is collaborating with human geneticists to understand how human mutations cause disease, and how these diseases can be modeled in mice. They are also collaborating with biochemists to develop novel ways of manipulating these proteins for therapeutic benefit.
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