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. 2016 Jun 3;311(2):L364–L374. doi: 10.1152/ajplung.00134.2016

Fig. 4.

Fig. 4.

Inhibition of tyrosine phosphorylation enhances surface levels of S1045Y-CFTR and improves its function. A: Western blot depicting the interaction of WT- and S1045Y-CFTR protein with Janus kinase 1 (JAK1). Bar graph on the right shows quantitation of interaction of JAK1 with CFTR. B: surface labeling assay to determine surface FLAG-WT-CFTR (left) and FLAG-S1045Y-CFTR (right) levels upon treatment with tyrosine kinase inhibitors as follows: ruxolitinib (5 μM), lapatinib (0.5 μM), or genistein (50 μM) following incubation with cyclohexamide (CHX). **P < 0.01. ns, Nonsignificant determined using Student's t-test for n = 3–4 experiments. C: left, representative traces of forskolin (Fsk)-stimulated S1045Y-CFTR-mediated Isc in CFBEo− cells following treatment with genistein (50 μM). Right, dot plot showing Fsk-stimulated Isc in response to various tyrosine kinase inhibitors quantified as normalized to untreated control S1045Y-CFTR-mediated currents. **P < 0.01 for genistein and *P < 0.05 for lapatinib determined using Student's t-test. No statistical significance could be established for imatinib and ruxolitinib treatment.