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. Author manuscript; available in PMC: 2011 Feb 5.
Published in final edited form as: Cell. 2010 Feb 5;140(3):338. doi: 10.1016/j.cell.2010.01.001

Figure 1. Regulation of PKR activity in obesity and lipid exposure.

Figure 1

(A) A genetic mouse model of obesity (ob/ob) was used to examine PKR activity by a kinase assay using immunopurified PKR and ATP [γ-32P] in white adipose tissue (WAT) and liver compared with age- and sex- matched lean controls. Fatty acid synthase (FAS) and β-tubulin proteins are shown as controls.

(B) PKR activity was examined in white adipose tissue (WAT) and liver of the male wild type mice kept either on regular diet (RD) or high fat diet (HFD) for 20 weeks.

(C) PKR activity in liver of 10 week-old male wild type mice, which were infused with lipid or saline for 5 hours. Total S6 protein is shown as control.

(D) PKR activity in primary MEFs. Cells were cultured in the absence or presence of 0.5 mM palmitic acid for 2 hours.

See also Supplemental Figure S1.