First published January 17, 2017 - More info
Diabetes is a disorder characterized by loss of β cell mass and/or β cell function, leading to deficiency of insulin relative to metabolic need. To determine whether stem cell–derived β cells recapitulate molecular-physiological phenotypes of a diabetic subject, we generated induced pluripotent stem cells (iPSCs) from subjects with maturity-onset diabetes of the young type 2 (MODY2), which is characterized by heterozygous loss of function of the gene encoding glucokinase (
Haiqing Hua, Linshan Shang, Hector Martinez, Matthew Freeby, Mary Pat Gallagher, Thomas Ludwig, Liyong Deng, Ellen Greenberg, Charles LeDuc, Wendy K. Chung, Robin Goland, Rudolph L. Leibel, Dieter Egli
Original citation: J Clin Invest. 2013;123(7):3146–3153. https://doi.org/10.1172/JCI67638
Citation for this retraction: J Clin Invest. 2017;127(3):1115. https://doi.org/10.1172/JCI92775
The corresponding authors were made aware of karyotype abnormalities through a routine quality control test of pluripotent stem cells used in the studies reported in this paper. After extensive internal review and genetic analysis, they found that the karyotypes of some of the cells used for the experiments reported were abnormal and that the normal karyotypes shown in Figure 1 and Supplemental Figure 2 were not from cell lines used in the study. They also cannot confirm the endonuclease-mediated correction of the mutant GCK G299R allele. H. Hua takes responsibility for the characterization and presentation of cell line karyotypes and the genetic manipulations. Because of these discrepancies, the authors wish to retract the article. They apologize for these errors and for any inconvenience caused to others.
See the related article at iPSC-derived β cells model diabetes due to glucokinase deficiency.