Egil Lien
University of Massachusetts Chan Medical School, MA·Microbiology & Immunology
Cells sometimes destroy themselves on purpose. This happens during normal development, and it is also a defense: when bacteria hide inside a cell, killing that cell removes their shelter and alerts the immune system.
- Fields
Microbiology & Immunology
Biochemistry
Biology
- Topics
cell death
pyroptosis
inflammation
- Grants
- 2 known grants, through May 2029
What they work on
- 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.
- Define how Raver1, Ptbp1 and other factors control RIPK1 by measuring RIPK1 RNA splicing, protein levels and nonsense-mediated decay (a system that destroys faulty RNA messages).
- Test whether Raver1-deficient mice show altered resistance to infection and inflammation, to learn how RNA splicing of RIPK1 shapes immune responses in a living animal.
- Determine how caspase-8 and caspase-1 signaling and gasdermin pore-forming proteins control clustering of the membrane protein Ninj1, using Yersinia infection, cytokines, inhibitors and expression systems.
- Test whether Ninj1 clustering and membrane rupture in myeloid immune cells are needed for host defense against Yersinia, using mouse infection models.
More about the research
Because cell death is so powerful, it has to be tightly controlled, and diseases can follow when it goes wrong. The lab studies the molecular switches and machinery behind cell death and inflammation in immune cells. Its model is infection with Yersinia, a bacterium that triggers these pathways in macrophages, immune cells that swallow microbes. One project looks at an early decision point in the pathway. The other looks at the final step, when the cell's outer membrane bursts open.
Why it matters
Many diseases arise when cell death and inflammation are poorly controlled, and bacterial infections depend on how well immune cells kill infected cells and sound the alarm. Learning how Raver1, Ptbp1 and Ninj1 control the RIPK1 hub and membrane rupture could reveal new targets for preventing or treating inflammatory disorders and infections where these pathways go wrong.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Congqing Wu
University of Kentucky, KY·Medicine & Clinical Research
Determine how NINJ1 in myeloid immune cells such as macrophages contributes to thrombosis. NINJ1 is the protein that actively ruptures the cell membrane during pyroptosis, an inflammatory form of cell death.
Markus Bosmann
Boston University, MA·Microbiology & Immunology
Test whether the signaling protein GNB2 protects against Legionella pneumonia by deleting it in mouse myeloid cells and alveolar macrophages, then profiling lung immune cells with CITE-Seq and Visium HD spatial transcriptomics.
Penghua Wang
University of Connecticut, CT·Microbiology & Immunology
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.
The school
University of Massachusetts Chan Medical School: 29 labs on PI Pages, $350M a year on research, 55 research doctorates a year.
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