Nature 409, 92–96 (2001).
In this Letter, we investigated the production and the phenotypic characterization of a SHIP2 (SH2 domain containing inositol phosphate 5-phosphatase type 2, or Inppl1) knockout mice. Total or partial loss of SHIP2 enzyme in these mice resulted in an increased insulin sensitivity. From these experiments, we concluded that SHIP2 is a potent negative regulator of insulin signalling and insulin sensitivity in vivo. However, we have recently realized that the 7.3-kilobase genomic DNA fragment deleted in these mice includes, in addition to exons 19–29 of the SHIP2 gene, the third (and last) exon of the Phox2a gene. The deletion of this exon results in the absence of the 124 carboxy-terminal amino acids from a total of 280, including part of the homeodomain, and should give rise to a completely non-functional Phox2a protein if expressed. As a consequence, the mice we described have both SHIP2 and Phox2a genes inactivated. It is currently unknown whether the increased insulin sensitivity we observed in our mice results from the inactivation of the SHIP2 gene alone, of the Phox2a gene alone, or of both genes.
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Clément, S., Krause, U., Desmedt, F. et al. Correction: Corrigendum: The lipid phosphatase SHIP2 controls insulin sensitivity. Nature 431, 878 (2004). https://doi.org/10.1038/nature03003
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DOI: https://doi.org/10.1038/nature03003
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