Deletion of Nicotinamide Nucleotide Transhydrogenase: A New Quantitive Trait Locus Accounting for Glucose Intolerance in C57BL/6J Mice. Diabetes 2006;55:2153–2156

In the article listed above, it was discovered that the Western blot in Fig. 1C was inappropriately manipulated. It appears that a protein band labeled C3H/HeH, which was a control sample, was added to the figure in its preparation. A Medical Research Council investigation found that there had been scientific misconduct by the first author, Dr. Helen Freeman, and that none of the other authors were involved. The other authors sincerely apologize for this having occurred, and wish to correct the published record. The authors have replicated the results of the original figure using their remaining bacterial artificial chromosome (BAC) mouse line (see Fig. 1C replacement below) and have also previously replicated the rescue of the glucose tolerance phenotype in this line, thus showing that the original conclusions of the article are not compromised.

New Fig. 1C legend: BAC transgenic expression of wild-type NNT protein in male C57BL/6J mice. Top panel: Expression of NNT protein in C3H/HeH (lane 1), C57BL/6J (lane 2), C57BL/6NTac (lane 3), and BAC transgenic C57BL/6J (lanes 4 and 5) mouse liver. Bottom panel: Reprobing of the same blot with an anti–α-tubulin antibody as a loading control. Protein was separated on a 4–12% gradient polyacrylamide gel (Invitrogen) and electrophoresed in MOPS SDS running buffer (NuPage, Invitrogen). The NNT antibody was our own custom affinity purified rabbit polyclonal. The anti–α-tubulin monoclonal antibody was 12G10. The 12G10 anti–α-tubulin antibody developed by Joseph Frankel and E. Marlo Nelsen was obtained from the Developmental Studies Hybridoma Bank, was developed under the auspices of the National Institute of Child Health and Human Development, and maintained by The University of Iowa, Department of Biology, Iowa City, IA. The Western blotting was carried out by Dr. Michelle Goldsworthy.

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