Arthur Gunzl
University of Connecticut, CT·Microbiology & Immunology
Trypanosoma brucei, Trypanosoma cruzi and Leishmania are single-celled parasites. They cause African sleeping sickness, Chagas' disease and leishmaniasis in millions of people.
- Fields
Microbiology & Immunology
Biochemistry
Genetics
- Topics
Trypanosoma brucei
Trypanosoma cruzi
Leishmania
- Grants
- 1 known grant, through Feb 2027
What they work on
- Determine how the cyclin-dependent kinase CRK9 controls spliced leader trans splicing in Trypanosoma brucei, including whether it phosphorylates the splicing factor TSR1, using parasites with chemically inhibitable analog-sensitive CRK9.
- Examine how blocking CRK9 disrupts assembly of the spliceosome, the RNA-protein machine that carries out splicing, in cultured T. brucei cells.
- Characterize CRK9's unusual three-part complex with an atypical L-type cyclin and a parasite-specific protein, and define a minimal active version that can be produced recombinantly for high-throughput inhibitor screens.
- Test whether CRK9 is the molecular target of SCYX-7158, a compound in clinical trials against African sleeping sickness.
More about the research
Drugs against these diseases are few and often toxic, and parasites are becoming resistant. These parasites make their messenger RNA in ways that differ sharply from human cells. Those differences are possible weak points for new drugs.
Why it matters
Patients with African sleeping sickness, Chagas' disease and leishmaniasis need safer drugs that parasites have not yet resisted. CRK9 is essential to a gene-expression step unique to these parasites, and its enzyme family is highly druggable. That makes it a promising drug target. A lab-produced CRK9 complex could enable screens for new inhibitors.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Christian Tschudi
Yale University, CT·Microbiology & Immunology
Determine how T. brucei parasites receive the signal to begin making the metacyclic VSG (mVSG) coat that lets them infect mammals, using parasites induced to develop by switching on the RNA-binding protein RBP6.
Evan Alexander Scott
University of Virginia, VA·Biomedical Engineering
Validate a combination nanotherapy that both dampens local immune attack on the heart and kills parasites, testing whether it treats established chronic Chagas cardiomyopathy without reactivating Trypanosoma cruzi.
Ruslan Afasizhev
Boston University, MA·Biochemistry
Define how complexes built around KRET1, an enzyme that adds U-tails to RNA, couple tailing with RNA degradation in the T. brucei mitochondrion, using proteomics, imaging, and cryo-EM.
The school
University of Connecticut: 31 labs on PI Pages, $434M a year on research, 360 research doctorates a year.
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