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. Author manuscript; available in PMC: 2020 Feb 1.
Published in final edited form as: J Leukoc Biol. 2019 Sep 1;107(2):175–183. doi: 10.1002/JLB.1HI0219-073RR

FIGURE 1. Generation of HL-60-β2 proline mutant cells and HL-60-talin-1 KO cells.

FIGURE 1

(A) Comparison of transmembrane domains (TMD) of human integrin β3 and β2 subunits. Sequence alignment in top panel. Proline mutant sites Ala711 in β3 and paralogous Leu697 in β2 highlighted in red. Bottom panel: 3D model of TMD of integrin β2 (red) compared to integrin β3 (grey). (B) β2 (CD18, top) and CXCR2 (bottom) expression on the surface of CXCR2-transfected HL-60 cells (HL60), these same HL-60 in which β2 integrin was knocked out (HL60-β2-KO), reconstituted with wild-type β2 (HL60-β2-WT) or with the kink mutant (HL60-β2-L697P), compared to talin-1 knockout HL-60 cells (HL60-talin-1 KO) cells. (C) Expression of talin-1 in parental or talin-KO HL-60 cells. β actin as loading control