Ryan Hanson
South Dakota State University, SD·Biology
When cells are damaged or stressed, they must choose a response: pause and repair, enter senescence (a permanent, non-dividing survival state), or die. Wrong choices are linked to inflammatory disease and cancer.
- Fields
Biology
Biochemistry
- Topics
c-Jun N-terminal kinase
stress signaling
cell fate
- Grants
- 2 known grants, through Apr 2028
What they work on
- 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.
- Determine how the phosphatase DUSP1 drives pulses of JNK activity that limit cell death as cells enter therapy-induced senescence, and use CRISPR screens to find key regulators of JNK-driven cell fates.
- Measure how mRNA stability shapes gene expression patterns driven by JNK and the transcription factor c-Jun, using metabolic labeling of mRNA decay and live-cell imaging of fluorescent reporters with mutated 3′ UTR sequences.
- Test how promoter sequences and transcription factor binding sites combine to shape gene expression over time after JNK activation, using systematic deletions in fluorescent reporters, and use the data to refine a computational model of JNK signaling.
More about the research
A key player is JNK, a stress-activated kinase, an enzyme that switches other proteins on by adding phosphate groups. Live-cell imaging shows that JNK activity rises and falls in patterns over time, and these patterns match different cell fates and gene activity. The two projects ask how individual cells read the timing and location of JNK activity, combining live-cell imaging, genetic tools and computational modeling.
Why it matters
Faulty cell fate decisions under stress are associated with inflammatory disease and cancer, and stress-signaling proteins are attractive drug targets. Knowing how JNK's timing and location decide between death, repair and senescence, including after cancer therapy, could inform ways to steer cell fates. The computational model of JNK signaling could also support future research on how cells process stress information.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Andrew Paek
University of Arizona, AZ·Biochemistry
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.
Diana Monsivais
Baylor College of Medicine, TX·Medicine & Clinical Research
Define how retinoic acid production by ALDH1A1 and ALDH1A3 controls stem cell regeneration and maturation in the endometrium, using new creERT2-tdTomato reporter mice for lineage tracing and transcriptomic studies in endometrial organoids.
John G. Albeck
University of California-Davis, CA·Biology
Use multiplexed live-cell sensors to constrain mathematical models of how glycolysis rates vary across single cells, and identify the smallest, most informative set of measurements.
The school
South Dakota State University: 3 labs on PI Pages, $82M a year on research, 46 research doctorates a year.
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