Penghua Wang
University of Connecticut, CT·Microbiology & Immunology
Sepsis happens when the body overreacts to an infection, usually a bacterial one, and its own inflammation damages organs. It causes more than 250,000 deaths a year in the United States and has no effective treatments.
- Fields
Microbiology & Immunology
Biochemistry
Medicine & Clinical Research
- Topics
sepsis
inflammasome
caspase-4
- Grants
- 1 known grant, through Jan 2031
What they work on
- Test whether unanchored lysine 48- and lysine 63-linked ubiquitin chains bind caspase-4/11 and promote its assembly and activation, using cell-free and biochemical assays.
- Determine how UBXN1 enriches and tethers free ubiquitin chains to caspase-4/11 during non-canonical inflammasome signaling, using biochemical, microscopy, genetic and pharmacological tools in cells.
- Define UBXN1's role in the progression of LPS-induced, polymicrobial and single-bacteria sepsis using genetically modified mouse models.
More about the research
One driver is the inflammasome, a large protein complex inside cells that senses infection and triggers inflammation and a fiery form of cell death called pyroptosis. Inflammasomes help fight bacteria, but when they stay overactive they harm tissues.
Why it matters
Sepsis kills more than 250,000 people a year in the U.S. and lacks effective therapies. By revealing how UBXN1 and free ubiquitin chains switch on the inflammation pathway that drives sepsis, this work could lay the groundwork for small-molecule drugs that block UBXN1. Such drugs might help treat sepsis and other autoinflammatory diseases.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Patrick Lombardi
Mount St. Mary's University, MD·Biochemistry
Identify the specific molecular contacts between the ASCC2 CUE domain, a small ubiquitin-binding module, and K63-linked polyubiquitin chains, using NMR spectroscopy to report on atom-level interactions.
Egil Lien
University of Massachusetts Chan Medical School, MA·Microbiology & Immunology
Determine how loss of the splicing factors Raver1 or Ptbp1 changes RIPK1/caspase-8-driven cell death and inflammation, using knockout macrophages and other cell lines infected with Yersinia.
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 Connecticut: 31 labs on PI Pages, $434M a year on research, 360 research doctorates a year.
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