The Borkan lab investigates pathways that promote renal cell survival and minimize acute kidney injury (AKI) after a variety of clinical insults, including ischemia and nephrotoxin exposure. The lab focuses on signaling pathways that mediate renal cell death in order to interrupt them and preserve organ function. The lab is currently investigating nucleophosmin, a link between rapid AKI diagnostics and peptide-based therapeutics that interrupt protein-protein interaction and significantly reduce AKI severity. The state-of-the art genetic screening and computational tools are used to identify AKI signaling pathways during nephrotoxic antibiotic exposure.  We are currently funded by the NIH (RO-1 DK118267A1) to study “Nucleophosmin Centered Diagnostics and Treatment of Ischemic Acute Kidney Injury”.

Five selected publications:

1. Wang Z et al. Nucleophosmin, a critical Bax cofactor in ischemia-induced cell death. Molecular and Cellular Biology, 2013. PMID: 23459946
2. Gall JM et al. Conditional knockout of proximal tubule mitofusin 2 accelerates recovery and improves survival after renal ischemia. Journal of the American Society of Nephrology, 2015. PMID: 25201884
3. Wang, Z et al. Nucleophosmin Phosphorylation as a Diagnostic and Therapeutic Target for Ischemic AKI. Journal of the American Society of Nephrology, 2019. PMID: 30573638
4. Igwebuike C et al. Cross Organelle Stress Response Disruption Promotes Gentamicin-Induced Proteotoxicity. Cell Death and Disease, 2020. PMID: 32245975
5. Wang et al. T95 Nucleophosmin Threonine 95 Phosphorylation as a Novel Mediator and Marker of Cell Death. American Journal of Physiology, 2020.