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Nathaniel Hathaway, PhD, is a UNC Lineberger Comprehensive Cancer Center member and Assistant Professor in the Eshelman School of Pharmacy at UNC-Chapel Hill. Hathaway Lab uses a combination of chemical-biology and cell-biology approaches to unravel the molecular mechanisms that govern gene expression.

Assistant Professor, School of Pharmacy
UNC-Chapel Hill
Molecular Therapeutics

Area of Interest

I created my lab at UNC with a founding idea that our group could make a unique contribution to understanding dynamic epigenetic processes by using unique chemical biology approaches I have pioneered. Through the combination of protein bioengineering, synthetic organic chemistry, and mammalian cell-based model systems, we have created and exploited platforms that use chemically tethered enzymatic recruitment to specific chromatin loci to produce a host of mechanistic insights. Additionally, we have used molecular pathway based high-throughput drug discovery methods to identify and refine chemical inhibitors of disease-relevant epigenetic pathways. As I look to the future with our maturing scientific research group, we will build on our track record of revealing mechanistic insights into mammalian gene regulation, but also harness our technologies in a translational sense to make significant inroads into new epigenetic based therapeutics with a focus on cancer. At this time, we have excelled in three specific and interrelated overarching projects:
  1. Mechanistic exploration of molecular determinants of heterochromatin formation and epigenetic memory, using chemical induced proximity (CIP) to recruit defined epigenetic regulators to chromatin in vivo assay (CiA) reporter systems in mammalian cells.
  2. Drug discovery campaigns to identify inhibitors of epigenetic pathways with relevance to human disease, using a focused epigenetically targeted compound set to run two distinct chromatin-based functional screens followed by molecular target identification and exploration of mechanism-of-action.
  3. Gene specific regulation of endogenous disease-relevant loci with chemical epigenetic modifiers (CEM)s, which harness endogenous epigenetically active enzymes and recruit them to specific genes targeted by deactivated Cas9 (dCas9).

Awards and Honors

  • 2017 CBMC Teaching Recognition Recipient
  • 2017 IBM Junior Faculty Development Award
  • 2016 CBMC Teaching Recognition Recipient
  • 2016 AACP – New Investigator Award Recipient
  • 2001 Undergraduate degree with distinction magna cum laude
  • 2000 Michelson-Morley Research Competition 1st Place

Find publications on PubMed