The main focus of my research is to delineate the mechanism by which kidney disease risk variants in APOL1 accelerate the progression of kidney disease in humans. We found that induced expression of APOL1 kidney disease variants in cell culture is associated with increased loss of cellular potassium and dysregulation of signaling pathways known to cause kidney failure. The ultimate goal of my research is to extend these findings and translate them into improved diagnostic and treatment approaches to chronic kidney disease.

Using APOL1 transgenic cell lines, transgenic APOL1 mice and specific chemical inhibitors we aim to fully characterize the effects of APOL1 risk variants on normal cellular signaling pathways. These robust systems will enable us to answer the question of how APOL1 risk variants result in cell death, and what protective mechanisms shield certain cells from APOL1 toxicity. We collaborate with Dr. Martin Pollak’s and Dr. David Friedman’s research groups at the Beth Israel Deaconess Medical Center.

As an initial step towards translating our findings to human kidney disease, we collaborate with nephrologists and pathologists nationwide who provide us with kidney biopsy samples from individuals with APOL1 nephropathy. These biopsy samples provide us with a platform for validating relevant signaling pathways discovered in cell culture and transgenic mice.


  1. Olabisi OA, Soto-Nieves N, Nieves E, Yang TT, Yang X, Yu RY, Suk HY, Macian F, Chow CW. Regulation of transcription factor NFAT by ADP-ribosylation. Mol Cell Biol. 2008; 28(9): 2860-71.
  2. Olabisi OA, Chow CW. Assay for protein modification by poly-ADP-ribose in vitro. Methods Mol Biol. 2011; 780:47-55.
  3. Olabisi OA, Zhang JY, VerPlank L, Zahler N, DiBartolo S 3rd, Heneghan JF, Schlondorff JS, Suh JH, Yan P, Alper SL, Friedman DJ, Pollak MR. APOL1 kidney disease risk variants cause cytotoxicity by depleting cellular potassium and inducing stress-activated protein kinases. Proc Natl Acad Sci U S A. 2016; 113(4):830-7.

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