Elizabeth Yeh
Indiana University-Purdue University-Indianapolis, IN·Pharmacology
A single enzyme, a protein kinase called HUNK, links this lab's work on two very different diseases: Alzheimer's disease and breast cancer. Kinases are enzymes that switch other proteins on or off by adding phosphate groups.
- Fields
Pharmacology
Neuroscience
Biochemistry
- Topics
protein kinase
autophagy
Alzheimer's disease
- Grants
- 2 known grants, through Feb 2028
What they work on
- Test whether the HUNK kinase, an autophagy-promoting enzyme, declines in the dorsal and ventral hippocampus in Alzheimer's disease, using human patient samples and 5XFAD mice.
- Determine whether a newly identified drug that activates HUNK reduces Alzheimer's-related pathology and reverses spatial memory and motivated behavior deficits in mouse models.
- Test whether targeting HUNK in breast cancer cells disrupts the paracrine signaling loop between tumor cells and tumor-associated macrophages (TAMs).
- Determine whether HUNK targeting shifts TAMs from tumor-promoting M2-like states toward anti-tumor M1-like states and limits tumor growth and metastasis.
More about the research
HUNK promotes autophagy, the cell's recycling system for clearing damaged proteins and parts. These projects ask whether turning HUNK up or down could slow brain degeneration in one disease and block tumor spread in the other.
Why it matters
People with Alzheimer's disease currently lack drugs that meaningfully improve symptoms; HUNK activation could become a new druggable target for slowing pathology and cognitive decline. In breast cancer, where most patients do not benefit from immune checkpoint inhibitors, targeting HUNK may offer a way to reverse macrophage-driven tumor growth and metastasis.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Jason Weber
Washington University in St Louis, MO·Biochemistry
Test whether the ARF tumor suppressor traps the RNA-editing enzyme ADAR1 in the nucleolus, a compartment inside the nucleus. This trapping would stop ADAR1 from holding back type I interferon alarm signaling in TNBC cells that lack working p53.
Pradipta Ghosh
University of California-San Diego, CA·Biochemistry
Determine how the modular domains of GIV, a scaffold protein linking G-protein switches, drive stem-like states, tumor growth and drug resistance in triple-negative breast cancers, using patient-derived organoids, tissue microarrays and mouse models.
Yaguang Xi
University of Georgia, GA·Pharmacology
Determine how the oncogenic microRNA miR-10b and its target gene NR4A3 contribute to the experimental compound LG007's activity against triple-negative breast cancer.
The school
Indiana University-Purdue University-Indianapolis: 25 labs on PI Pages, $89M a year on research, 120 research doctorates a year.
More about Indiana University-Purdue University-Indianapolis
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