Mukesh Nyati Laboratory


Professor Nyati received his PhD from the University of Rajasthan, Jaipur, India and post-doctoral training in Dr. Ted Lawrence’s laboratory at the University of Michigan. Dr. Nyati has been working on basic and translational as well as clinical aspects of EGFR signaling.  In the laboratory, Dr. Nyati is working on developing novel therapeutic agents including cell permeable peptides and their structural analogues to degrade EGFR. The main objective of this work is to sensitize tyrosine kinase inhibitor (TKI) resistant EGFR-driven tumors by promoting tumor specific EGFR degradation through blocking EGFR dimers and EGFR- Hsp90 interactions. Dr. Nyati is also working in collaboration with both basic scientists and clinicians in the head and neck SPORE program(link is external) at the University of Michigan to discover novel biomarkers of “response” to molecularly targeted therapy. The long-term goal of this research is to identify patients who are likely to respond to molecularly targeted therapies in combination with chemotherapy and/or radiotherapy early in the course of treatment so that the combination regimen is optimized.

Key Publications

  • Elaimy AL, Ahsan A, Marsh K, Pratt WB, Ray D, Lawrence TS, Nyati MK. ATM is the primary kinase responsible for phosphorylation of Hsp90α after ionizing radiation. Oncotarget, 7(50):82450-82457, 2016
  • Ray D, Cuneo KC, Rehemtulla A, Lawrence TS, Nyati MK. Inducing Oncoprotein Degradation to Improve Targeted Cancer Therapy. Neoplasia, 17(9):697-703, 2015.
  • Ahsan A, Ray D, Ramanand SG, Hegde A, Whitehead C, Rehemtulla A, Morishima Y, Pratt WB, Osawa Y, Lawrence TS, Nyati MK. Destabilization of the epidermal growth factor receptor (EGFR) by a peptide that inhibits EGFR binding to heat shock protein 90 and receptor dimerization. Journal of Biological Chemistry, 288:26879-86, 2013. PMCID:PMC3772236 
  • Ahsan A, Ramanand SG, Bergin IL, Zhao L, Whitehead CE, Rehemtulla A, Ray D, Pratt WB, Lawrence TS, Nyati MK. Efficacy of an EGFR-specific peptide against EGFR-dependent cancer cell lines and tumor xenografts. Neoplasia, 16:105-14, 2014. PMCID:PMC3978391.