Lisa C Burnett

Induced pluripotent stem cells (iPSC) created from skin fibroblasts of patients with Prader-Willi syndrome (PWS) retain the molecular signature of PWS.

D. J. Driscoll, D. Egli, B. Levy, 2016, Stem cell research.

Regulation of intracellular signaling and neuron function by Bardet-Biedl Syndrome proteins in patient-specific iPSC-derived neurons

D. Zheng, S. Tsang, D. Egli, 2020, bioRxiv.

Determination of the half life of circulating leptin in the mouse

R. Leibel, C. Leduc, A. Skowronski, 2016, International Journal of Obesity.

Loss of the imprinted, non-coding Snord116 gene cluster in the interval deleted in the Prader Willi syndrome results in murine neuronal and endocrine pancreatic developmental phenotypes

R. Leibel, C. Leduc, Lisa C Burnett, 2017, Human molecular genetics.

Loss of MAGEL2 in Prader-Willi syndrome leads to decreased secretory granule and neuropeptide production

J. Diedrich, J. Yates, M. Talkowski, 2020, JCI insight.

Hypomorphism of Fto and Rpgrip1l causes obesity in mice.

D. Storm, D. Egli, Pumin Zhang, 2016, The Journal of clinical investigation.

Human oocytes reprogram adult somatic nuclei of a type 1 diabetic to diploid pluripotent stem cells

N. Benvenisty, D. Egli, M. Sauer, 2014, Nature.

Deficiency in prohormone convertase PC1 impairs prohormone processing in Prader-Willi syndrome

D. J. Driscoll, K. Clément, D. Egli, 2016, The Journal of clinical investigation.