Steven Baker
Loyola University Chicago, IL·Microbiology & Immunology
When a virus infects a cell, the cell switches on a set of defense genes within minutes. Influenza virus, which sickens and kills people worldwide every year, must get past these defenses to replicate.
- Fields
Microbiology & Immunology
Biochemistry
Genetics
- Topics
influenza virus
ncISG15
interferon stimulated genes
- Grants
- 1 known grant, through Jul 2028
What they work on
- Determine whether the drop in the influenza NP protein, a core viral genome-packaging protein, caused by non-canonical ISG15 (ncISG15) reflects faster protein turnover, RNA turnover, or both.
- Test how the influenza interferon antagonist NS1 reduces ncISG15 levels, distinguishing effects on ncISG15 protein stability from effects on its messenger RNA.
- Define the host and viral proteins that interact with ncISG15 using proteomics, to identify which partners drive its antiviral activity independently of protein tagging (ISGylation).
- Characterize how ncISG15 restricts influenza genomic replication and progeny virus production in infected cells, comparing it with canonical ISG15.
More about the research
One of the most abundantly produced defense genes in humans is ISG15. Over about fifty years of study it has been tied to antiviral defense, immune balance and tumor formation, acting in several ways: as a tag attached to other proteins (a process called ISGylation), as a free protein inside cells that dampens interferon signaling, and as an inflammatory signal released outside cells. But genes are not simply on or off — a single gene can be cut and pasted into several different messenger RNA versions, called isoforms, through alternative RNA splicing, and these versions can encode different proteins.
Why it matters
Influenza causes heavy illness worldwide each year, and defining how a newly found form of ISG15 blocks the virus could point to new drug targets for reducing that burden. Because ISG15 is also involved in immune regulation and cancer biology, findings may extend to those conditions. More broadly, the work tests whether alternative RNA splicing is an overlooked source of antiviral defense molecules.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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The school
Loyola University Chicago: 8 labs on PI Pages, $61M a year on research, 156 research doctorates a year.
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