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. 2020 Sep 14;117(39):24326–24335. doi: 10.1073/pnas.2009078117

Fig. 4.

Fig. 4.

Bcr-Abl elevates integrin-mediated cell adhesion in a K3-dependent manner. (A) Protein expression of Bcr-Abl, c-Abl, murine K3, human K3 (rescue), and GAPDH by 32D myeloblasts with or without Bcr-Abl expression (BA+ or BA−), with or without Fermt3 gene deletion (K3+ or K3−), and with or without human K3 reexpression (rescue). (B) 32D cell adhesion to FN (n = 9), VCAM-1 (n = 6), or ICAM-1 (n ≥ 9) under static conditions. (C) 32D cells stably adhering to FN or VCAM-1 under flow (n ≥ 7). (D) 32D cell chemotaxis toward CXCL12 with or without preincubation with imatinib overnight (n ≥ 6). (E) 9EG7 staining intensities in 32D cells plated on FN (n ≥ 33) or VCAM-1 (n ≥ 49). Statistics by Kruskal–Wallis test. (F and G) K3 and Talin-1 mRNA (F; n ≥ 9) and Bcr-Abl, c-Abl, p-CrkL, K3, Talin-1, and GAPDH protein (G; n = 5) expression in 32D cells with or without 24-h imatinib treatment. Data are shown as mean ± SD. Statistics by one-way ANOVA, Tukey’s multiple-comparison test if not indicated otherwise. *P < 0.05, **P < 0.01, and ***P < 0.001.