Chongwoo Kim
Midwestern University-Glendale, AZ·Biochemistry
Cells must keep the wrong genes switched off, and protein machines called Polycomb complexes help do this by chemically marking chromatin, the packaged form of DNA. When Polycomb repressive complex 1 (PRC1) goes wrong, cancer can result.
- Fields
Biochemistry
Biophysics
Genetics
- Topics
Polycomb repressive complex 1
epigenetics
chromatin
- Grants
- 1 known grant, last ended Aug 2026
What they work on
- Systematically characterize secondary protein-protein interactions that act as selective checkpoints in assembling distinct PRC1 complexes, using X-ray crystallography, analytical ultracentrifugation and biolayer interferometry.
- Test how these secondary interactions determine which combinations of PRC1 proteins assemble, explaining how one binding interface influences the partner choice at another.
- Assess the functional effects of these interactions on PRC1 activity using a new FRET-based assay that measures histone modification.
More about the research
Human PRC1 is not a single machine but a family of complexes built from different combinations of related proteins, and the mix changes as cells specialize. A key unanswered question is why some protein combinations assemble while others do not.
Why it matters
Faulty Polycomb complexes can lead to cancer. Understanding how they normally form may guide the development of drugs that target them in cancer cells. The findings may also apply to other gene-regulating systems built from interchangeable related proteins.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Emily Dykhuizen
Purdue University, IN·Biochemistry
Develop CBX8 chromodomain inhibitors with improved cell permeability by selecting focused DNA-encoded libraries — small-molecule collections barcoded with DNA — designed for cellular activity rather than binding affinity alone.
James Palis
University of Rochester, NY·Biology
Test whether BMI1 and RING1B, proteins that silence genes by packaging chromatin, sustain self-renewal of human self-renewing erythroblasts by controlling gene activity epigenetically.
Nicholas Woods
University of Nebraska Medical Center, NE·Medicine & Clinical Research
Test whether Tazemetostat, which blocks the gene-silencing complex PRC2, prevents chemotherapy-induced shifts in tumor subtype, using organoids grown from tumors of Black and White PDAC patients.
The school
Midwestern University-Glendale: 2 labs on PI Pages, $14M a year on research.
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