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1C; mean values of V0.5 were ?36.0 �� 2.6 mV in control cells and ?37.1 �� 1.1 and ?37.3 �� 2.3 mV, respectively, in 20 and 40 nm rMIF-treated cells, n= 6 cells, P > 0.05), but rMIF was found Akt inhibitor to shift the activation curve significantly to the right [corresponding to V0.5 values of ?37.7 �� 0.8 mV for control cells, ?30.8 �� 2.0 mV for 20 nm rMIF (n= 6, P 0.05) and 40 nm rMIF, respectively (n= 6, P > 0.05). This indicated that rMIF did not alter the recovery of ICa,T from inactivation (Fig. 1D). Recombinant MIF also reduces the channel density by downregulating channel expression in HL-1 cells To investigate the effect of rMIF on the expression of atrium-derived cell channels, we measured the gene expression levels of TCC ��1G and ��1H before and after Montelukast Sodium rMIF treatment (Fig. 3). The TCC ��1G and ��1H subunit gene expression levels were normalized to ��-actin in each sample. The TCC ��1G and ��1H subunit mRNA levels were both decreased after 40 nm rMIF treatment (1.0 versus 0.55 �� 0.12 for TCC ��1G, P EPZ-6438 solubility dmso 27% of myocytes (n= 3), genistein inhibited ICa,T slightly or had no significant effect. Currents returned almost completely to baseline levels after washout of genistein in HL-1 cells (Fig. 4A). To differentiate between distinct PTK families, the effect of Src kinase inhibition on ICa,T was tested using PP1, which is a pyrazolopyrimidine derivative and specific inhibitor of the Src family of cytoplasmic non-receptor PTKs. Application of PP1 to HL-1 cells led to a similar increase in ICa,T to that observed with genistein (from ?22.0 �� 2.4 to ?36.3 �� 4.6 pA pF?1, n= 10 cells, P