Andrew Paek
University of Arizona, AZ·Biochemistry
Hydrogen peroxide (H2O2) is a reactive form of oxygen that cells make and encounter all the time. In small amounts it acts as a useful signal, a state called oxidative eustress.
- Fields
Biochemistry
Biology
Biophysics
- Topics
oxidative stress
hydrogen peroxide
redox signaling
- Grants
- 1 known grant, through Jun 2030
What they work on
- Identify proteins directly oxidized by high doses of H2O2 that switch on Group 2 stress proteins (FOXO1, NF-κB, GCN2) and block Group 1 proteins (p53, NRF2, AKT), using a targeted approach in human cells.
- Map which reactive cysteines, sulfur-containing amino acids, are oxidized at different H2O2 doses, using unbiased proteomics paired with phosphoproteomics to reveal how oxidation changes kinase activity.
- Test three competing models of how PRDX proteins, enzymes that break down peroxide, selectively control which cellular proteins become oxidized.
- Determine how H2O2-driven redox signaling affects gut homeostasis, using a human colonic monolayer, a flat sheet of colon cells developed by the lab.
More about the research
In large amounts it causes damage and disease, a state called oxidative distress. How a cell tells these two situations apart, and which of its proteins react to each, is still poorly understood. The question matters for diseases such as cancer and ischemia-reperfusion injury, the tissue damage that occurs when blood flow returns after a blockage.
Why it matters
Oxidative stress contributes to diseases such as cancer and ischemia-reperfusion injury. By identifying the molecular switches that separate mild, beneficial oxidative stress from toxic stress, this work could point to new therapeutic targets for treating oxidative stress-related diseases. The colon model could also clarify how this signaling affects gut health.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Kristofer Fritz
University of Colorado Denver/Anschutz Medical Campus, CO·Pharmacology
Characterize how chronic alcohol metabolism changes thiol redox signaling, the on-off switching of cysteine residues in proteins, in liver cells, using redox proteomics and bioinformatics.
Ryan Hanson
South Dakota State University, SD·Biology
Test whether the length of time JNK, a stress-activated kinase, stays at mitochondria decides mitochondrial damage, reactive oxygen species production and cell death, using optogenetic tools to control JNK's location over time.
Savas Tay
University of Chicago, IL·Biomedical Engineering
Determine how sentinel cells encode information about pathogens and stress in cytokine dynamics, including memory of prior stimuli and causes of cytokine overproduction, using single-cell secretion assays and live-cell analysis.
The school
University of Arizona: 36 labs on PI Pages, $1.0B a year on research, 487 research doctorates a year.
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