Enhanced ERK-1/2 activation in mice susceptible to coxsackievirus-induced myocarditis
J. Clin. Invest. Mary Anne Opavsky, et al. 109:1561 doi:10.1172/JCI13971 [Go to this article.]

Figure 2
Activation of the ERK-1/2 pathway by CVB3 infection is dependent on p56^Lck (Lck). (a) Jurkat cells or JCaM cells (10⁷) were incubated with CVB3 (moi = 50; +) or control media (–) for 5 or 10 minutes, then lysed. One result represents three experiments. (b) Jurkat, JCaM, and JCaM cells with control vector (JCaM/vector) or Lck restored (JCaM/Lck) (10⁷) were incubated with CVB3 (moi = 50; +) or control media (–) for 5 minutes, then lysed. One result represents two experiments. (c) TCR-β chain negative Jurkat cells (10⁷) were lysed after incubation for 5 or 10 minutes with CVB3 (moi = 50; +) or control media (–), then lysed. One result represents two experiments. All cell lysates were immunoblotted with anti–phospho-ERK-1/2 (P-ERK-1/2) and anti–total ERK-1/2 Ab’s. Fold change in P-ERK-1/2-total ERK-1/2 ratio is indicated. (d) CVB3 binding to T cell lines does not require activation of ERK-1/2. Jurkat and JCaM cells (5 × 10⁶) were incubated with [³⁵S]-CVB3 for 1 hour in the presence (PD98059) or absence (DMSO) of MEK-1/2 inhibitor. Binding of virus is expressed as mean percentages (± SEM) for triplicate cultures. Viral binding to JCaM cells was twice as high as binding to Jurkat cells (*P = 0.0001; Student t test).