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Corrigendum

Volume 54, September 2006

Pages E536–E543: Chaodong Wu, Salmaan A. Khan, Li-Jen Peng, Honggui Li, Steven G. Carmella, and Alex J. Lange. Perturbation of glucose flux in the liver by decreasing fructose-2,6-bisphosphate levels causes hepatic insulin resistance and hyperglycemia.

The authors thank an alert reader for pointing out the missing information on the generation of a kinase-deficient 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (6PFK2/FBP2 or Bif-KD). In the text of the paper, the authors cited their paper in Endocrinology (5), mainly for adenovirus preparation, i.e., amplification and purification. Strictly speaking, what was not provided was the information on the generation of the mutated cDNA coding for the kinase-deficient 6PFK2/FBP2. This information was presented at the 2002 American Diabetes Association Scientific Meeting, and the abstract was published in the supplemental issue of Diabetes (4). This abstract was cited in their Endocrinology paper, as well as in a paper from their collaborator (1). It appears that this abstract was not accessible.

Herein is provided the information for generation of the mutated cDNA coding for the kinase-deficient 6PFK2/FBP2. One mutation was made that changed Ser³² to asparatate; another mutation was made that changed Thr⁵⁵ to valine. These manipulations were chosen on the basis of papers published in J Biol Chem (2, 3). The mutated cDNA was then packaged into adenovirus using a commercial kit from Qbiogene (Carlsbad, CA). This mutated cDNA was also overexpressed in heart of transgenic mice (1).

The authors want to point out that they did not publish any paper in Molecular Cell.

REFERENCES

1. Donthi RV, Ye G, Wu C, McClain DA, Lange AJ, Epstein PN. Cardiac expression of kinase-deficient 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase inhibits glycolysis, promotes hypertrophy, impairs myocyte function, and reduces insulin sensitivity. J Biol Chem 279: 48085–48090, 2004.[Abstract/Free Full Text]
2. Kurland IJ, El-Maghrabi MR, Correia JJ, Pilkis SJ. Rat liver 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase. Properties of phospho- and dephospho-forms and of two mutants in which Ser32 has been changed by site-directed mutagenesis. J Biol Chem 267: 4416–4423, 1992.[Abstract/Free Full Text]
3. Vertommen D, Bertrand L, Sontag B, Di Pietro A, Louckx MP, Vidal H, Hue L, Rider MH. The ATP-binding site in the 2-kinase domain of liver 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase. Study of the role of Lys-54 and Thr-55 by site-directed mutagenesis. J Biol Chem 271: 17875–17880, 1996.[Abstract/Free Full Text]
4. Wu C, Okar DA, Peng L, Lange AJ. Decreasing fructose-2,6-bisphosphate leads to diabetic phenotype in normal mice (Abstract). Diabetes 51, Suppl 2: 1300, 2002.
5. Wu C, Okar DA, Stoeckman AK, Peng L, Herrera AH, Herrera JE, Towle HC, Lange AJ. A potential role for fructose-2,6-bisphosphate in the stimulation of hepatic glucokinase gene expression. Endocrinology 145: 650–658, 2004.[Abstract/Free Full Text]

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