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. 2015 Mar 30;112(15):4642–4647. doi: 10.1073/pnas.1423201112

Fig. 3.

Fig. 3.

Disruption of the JAK2 JH2 ATP binding site is distinct from structural disruption. (A) JAK2(Y1007–Y1008) phosphorylation of JAK2 mutants in the presence of type I cytokine receptor (EPOR) in γ2A cells. Basal JAK2 phosphorylation in the absence of EPOR expression is shown on the left. (B) STAT5A(Y694) phosphorylation from the same samples as pJAK2 in A. Phosphorylation was measured from whole-cell lysates of transfected γ2A cells using immunoblotting and normalized to JAK2-HA and STAT5-HA expression levels, respectively. Expression levels of EPOR were analyzed by immunoblotting with anti-HA and found to be equal. (C) STAT1(Y701) phosphorylation of endogenous STAT1 in γ2A cells. Bar graph shows quantification of pSTAT1 from immunoblots normalized to basal pSTAT1 levels in cells transfected with wild-type JAK2 (leftmost sample). Actin is shown as a loading control. All error bars are SDs from three independent experiments.