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. Author manuscript; available in PMC: 2011 Jul 1.
Published in final edited form as: Biochim Biophys Acta. 2010 May 2;1802(7-8):593–600. doi: 10.1016/j.bbadis.2010.04.008

Fig 2.

Fig 2

A: Knock out of LKB1 did not affect expression of the fatty acid transporter protein CD36 (N=11–12). B: Phosphorylation of ACC was blunted in LKB1-KO hearts during both basal and ischemic conditions (a: P<0.01, b: P<0.05 vs. basal.*: P<0.05 vs. control, N=6–8). ACC protein-expression was similar among genotypes. C: The activity of ACC was measured in the presence or absence of 10 mM citrate in protein lysates from perfused hearts after reperfusion. There were no differences in activity among genotypes (N=5–6). D: Expression of MCD was reduced by ~70% in LKB1-KO hearts (P<0.05 vs. control (N=6).