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. Author manuscript; available in PMC: 2010 Feb 9.
Published in final edited form as: J Proteome Res. 2009 Oct;8(10):4823. doi: 10.1021/pr900561g

Figure 6.

Figure 6

Predicted outcome of KATP channel deficit and functional validation. (A) “Cardiovascular disease” was significantly overrepresented as a consequence of KATP channel deficit based on Ingenuity Pathways Analysis of both the KATP channel-dependent altered proteins (Proteome) and their derived protein network (Interactome). (B–D) Functional confirmation of predicted outcome. While wild-type (WT) and Kir6.2-knockout (KO) counterparts exhibited no difference in structural or functional parameters in the absence of imposed stress, progressively greater challenge by mild (chronic repetitive aquatic exercise), moderate (deoxycorticosterone acetate/salt-induced hypertension) or severe (transverse aortic constriction) stress led to aggravated increases in left ventricular (LV) mass (B; *P < 0.05) and decreases in LV fractional shortening, FS (C; *P < 0.05, **P < 0.01), with KATP channel deletion ultimately leading to decreasing post-stress survival (D; **P < 0.01 versus WT).