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. 2011 Jan 21;60(2):486–495. doi: 10.2337/db10-0650

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© 2011 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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FIG. 1. — Generation and characterization of aP2-dn-JNK transgenic (Tg) mice. A: Schematic representation of the aP2-dn-JNK transgenic construct. The dn-JNK cDNA, in which lysine 149 in the ATP domain of the JNKK2 moiety was replaced by Met to create the HA-JNKK2(K149M)JNK1, was subcloned downstream of the 5.4-kb aP2 promoter/enhancer and upstream of the hGH polyadenylation signals. B: Detection of the dn-JNK transgene by PCR analysis in mice. Specific fragments of 653 bp spanning from the aP2 promoter to the JNKK2 gene was amplified. ^−/−, transgene negative; ^−/+, transgene positive; L, 1-kb DNA ladder; PC, plasmid DNA positive control; WT, wild-type littermates. C: Expression of the dn-JNK transgene by RT-PCR. The presence of the dn-JNK mRNA was analyzed in various tissues of aP2-dn-JNK transgenic mice (10 weeks old) by RT-PCR using specific primers for the dn-JNK transgene (n = 5). EPI, epididymal adipose fat; PRF, perirenal fat; SU, subcutaneous adipose fat. D: Confirmation of the dn-JNK protein expression by immunoblotting (n = 4). Protein extracts from various tissues were subjected to Western blotting with anti-HA antibody.