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J. Biol. Chem., Vol. 281, Issue 5, 2649-2653, February 3, 2006
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RIP-Cre Revisited, Evidence for Impairments of Pancreatic 
-Cell Function*
1
13
From the
Laboratory of Genetics and Physiology, NIDDK, National Institutes of Health, Bethesda, Maryland 20892, the German Institute of Human Nutrition Potsdam-Rehbruecke and Department of Human Nutrition, University of Jena, Jena D-07743, Germany, the ¶Howard Hughes Medical Institute, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, and the ||Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-0615
The Cre/loxP recombinase system for performing conditional gene targeting experiments has been very useful in exploring genetic pathways that control both the development and function of pancreatic 
-cells. One particular line of transgenic mice (B6.Cg-Tg(Ins2-cre)25Mgn/J), commonly called RIP-Cre, in which expression of Cre recombinase is controlled by a short fragment of the rat insulin II gene promoter has been used in at least 21 studies on at least 17 genes. In most of these studies inactivation of the gene of interest was associated with either glucose intolerance or frank diabetes. Experimental evidence has been gradually emerging to suggest that RIP-Cre mice alone display glucose intolerance. In this study experiments from three laboratories demonstrate that RIP-Cre mice, in the absence of genes targeted by loxP sites, are glucose intolerant, possibly due to impaired insulin secretion. In addition, we review the use of RIP-Cre mice and discuss possible molecular underpinnings and ramifications of our findings.
Received for publication, November 17, 2005
* This work was supported in part by grants from the Deutsche Forschungsgemeinschaft (to M. R.) and the Fritz-Thyssen-Stiftung (to M. R.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 Both authors were supported by the Intramural Research Program of the National Institutes of Health (NIDDK).
2 To whom correspondence may be addressed. E-mail: mark.magnuson{at}vanderbilt.edu. 3 To whom correspondence may be addressed: Laboratory of Genetics and Physiology, NIH/NIDDK, 8 Center Dr., Rm. 101, Bethesda, MD 20892-0822. Tel.: 301-496-2716; Fax: 301-480-7312; E-mail: lotharh{at}mail.nih.gov.
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