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. 2021 Jan 27;112(3):1225–1234. doi: 10.1111/cas.14786

FIGURE 6.

FIGURE 6

Kinase domain of ROR1 is required for geldanamycin (GA)‐induced proteasome degradation. Western blot analysis of ROR1 in COS‐7 cells transfected with ROR1 WT, (A) a deletion mutant of entire kinase domain (ROR1‐△TK) and the C‐terminal region (ROR1‐△ST1 + P+ST2), and (C) a kinase‐dead mutant (ROR1 K558R), in the presence or absence of 0.5 μmol/L GA for 24 h. Immunoprecipitation‐western blot analysis using ROR1 Ab in COS‐7 cells transfected with ROR1 WT, (B) ROR1‐△TK and ROR1‐△ST1 + P+ST2, and (D) a kinase‐dead mutant (ROR1 K558R). E, Western blot analysis of ROR1 in COS‐7 cells with overexpressing ROR1 (left panel) and PC‐9 cells (right panel), treated with 0.5 μg/mL tunicamycin for 12 h in the presence or absence of 0.5 μmol/L GA. In (A) to (E), β‐actin served as a loading control. CRD, cysteine‐rich domain; Ig, Ig‐like domain; P, proline‐rich domain; ST, serine/threonine‐rich domain; TK, tyrosine kinase domain; VC, vector control