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Work Arrangement: 
Requisition Number:  206890
Regular or Temporary:  Regular

Durham, NC, US, 27710

Personnel Area:  MEDICAL CENTER
Date:  May 28, 2023
School of Medicine Established in 1930, Duke University School of Medicine is the youngest of the nation's top medical schools. Ranked sixth among medical schools in the nation, the School takes pride in being an inclusive community of outstanding learners, investigators, clinicians, and staff where interdisciplinary collaboration is embraced and great ideas accelerate translation of fundamental scientific discoveries to improve human health locally and around the globe. Composed of more than 2,500 faculty physicians and researchers, more than 1,300 students, and more than 6,000 staff, the Duke University School of Medicine along with the Duke University School of Nursing, Duke University Health System and the Private Diagnostic Clinic (PDC) comprise Duke Health. a world-class academic medical center. The Health System encompasses Duke University Hospital, Duke Regional Hospital, Duke Raleigh Hospital, Duke Primary Care, Duke Home and Hospice, Duke Health and Wellness, and multiple affiliations.


Postdoctoral position available immediately for research on genome editing in rare genetic diseases. Genome editing with adeno-associated virus vectors is a major focus of the laboratory. The project will include invivo genome editing to treat glycogen storage disease (GSD), either GSD typeIa or Pompe disease.  A second focus is to develop small molecules to stimulate autophagy and reverse the abnormalities of autophagy in GSD. New drug therapy for GSD will have implications for the treatment of more common conditions, including non-alcoholic fatty liver disease and diabetic nephropathy. Representative publications describe the scope of this project.1-6 Duke University features outstanding clinical and scientific resources with opportunities for local and international collaboration. This position will support an active collaboration with established genome editing, autophagy, andvirology research groups. Candidates with molecular biology experience, and familiarity with viral vectors, immunology, and/or biochemistry are encouraged to apply. Ph.D. and/or M.D. required.  The position is located in Dwight Koeberl's laboratory in the Department of Pediatrics and Division of Medical Genetics, and the Molecular Genetics and Microbiology Department at Duke University.

Website: https ://scholars.duke.edu/display/per3329362

Interested candidates should submit their electronic application to dwight.koeberl@duke.edu that should include: (1) the names of 3 references, and (2) an updated CV.



1            Farah,B. L. et al. Inducti on of autophagy improves hepatic lipid metabolism in glucose-6-phosphatas e deficiency. J Hepatol 64, 370-379, doi:10.10 16/j.jhep.2015.10.008 (2016).

2            Farah, B. L. et al. Hepatic mitochondrial dysfunction is a feature of Glycogen Storage Disease Type Ia (GSDIa). Sci Rep7, 44408, doi: 10.1038/srep44408(2017).

3            Landau, D. J. et al. In Vivo Zinc Finger Nuclease-mediated Targeted Integration of a Glucose -6-phosphatase Transgene Promotes Survival in Mice With Glycogen Storage Disease Type IA. Mol Ther 24, 697-706, doi:10. 1038/mt.2016.35(2016).

4            Waskowicz, L. R. et al. Bezafibrate induces autophagy and improves hepatic lipid metabolism in glycogen storage disease type Ia. Hum Mol Genet 28,143-154, doi:10.1093/hmg/ddy343 (2019).

5            Kang, H . R. et al. Bezafibrate Enhances AAV Vector-Mediated Genome Editing in Glycogen Storage Disease Type Ia. MolTher Methods Clin Dev 13,265-273, doi:10.1016/j.omtm.2019.02.002 (2019).

6            Yavarow, Z. A. et al. Fenofibrate rapidly decreases hepatic lipid and glycogen storage in neonatal mice with glycogen storage disease type Ia. Hum MolGenet 29, 286 -294, doi:10.1093/hmg/ddz290 (2020).


Minimum Qualifications



See job description for education requirements.



See job description for requirements.


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