Emily Troemel
University of California-San Diego, CA·Microbiology & Immunology
Cells under attack from viruses and other pathogens that live inside cells must both fight the invader and protect their own proteins from damage. Both projects center on the Intracellular Pathogen Response (IPR), a gene program the lab discovered in the nematode worm C.
- Fields
Microbiology & Immunology
Genetics
Biochemistry
- Topics
C. elegans
nematode
innate immunity
- Grants
- 2 known grants, through Dec 2027
What they work on
- Determine where and how the RIG-I-like receptor DRH-1 promotes defense against Orsay virus in C. elegans intestinal epithelial cells, including how it senses viral replication and triggers the IPR.
- Identify the signaling pathway activated downstream of DRH-1 in C. elegans, which lacks interferons and their usual signaling partners.
- Determine which host cells, including uninfected bystander cells, mount an antiviral immune response to Orsay virus infection in C. elegans.
- Determine how SKR-3, SKR-4, SKR-5, FBXA-75 and FBXA-158 pair up and interact within the CUL-6 ubiquitin ligase, including redox-dependent pairing, using in vitro and in vivo approaches.
- Identify the proteins targeted by the CUL-6 ubiquitin ligase and trace their fate, testing whether they are degraded in the lysosome through autophagy factors to boost heat tolerance.
More about the research
elegans. The IPR switches on in intestinal cells during infection. One project asks how the IPR is triggered to fight RNA viruses. The other asks how it protects proteostasis, the cell's ability to keep its proteins correctly folded and in balance.
Why it matters
RNA viruses, from SARS-CoV-2 to common endemic infections, often first infect the epithelial cells lining the gut and airways. Revealing new ways these cells detect and signal viral infection could inform new treatments for RNA virus infections and inflammatory diseases. A heat-protective protein-disposal pathway could also suggest strategies for aging-related diseases linked to protein misfolding.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Patrick Mitchell
University of Washington, WA·Microbiology & Immunology
Map the host and viral determinants required for rotavirus NSP1, a non-structural protein that suppresses interferon responses, to trigger activation of the human NLRP1 inflammasome.
Karen Swanson
University of North Carolina at Chapel Hill, NC·Microbiology & Immunology
Define the mechanism by which the human protein STING, normally an antiviral sensor, acts as a host factor supporting genome replication of rhinovirus species RV-A and RV-C but not RV-B.
Chen Shen
Washington University in St Louis, MO·Biophysics
Characterize functionally how HIV-1 Gag and its matrix (MA) region bind the CARD8 inflammasome sensor to prevent its activation by the viral protease, and compare the strength of this inhibition across matrix proteins from different HIV-1 subtypes.
The school
University of California-San Diego: 84 labs on PI Pages, $1.9B a year on research, 637 research doctorates a year.
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