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. 2021 Jan 4;12:51. doi: 10.1038/s41467-020-20259-0

Fig. 1. BCR-ABL regulates USP47 through RAS/ERK and STAT5 pathway in CML.

Fig. 1

a mRNA levels of DUBs in bone marrow (BM) mononuclear cells from primary CML patients compared with normal BM CD34+ cells (CML n = 5, normal n = 3 biologically independent samples). Data are presented as mean ± s.d. *p < 0.05; **p < 0.01; ***p < 0.001, using two-sided Student’s t-test. b USP47 and BCR-ABL protein expression were measured by western blot in primary CML cells at different clinical stages compared with normal BM CD34+ cells. NM normal BM, CP chronic phase, AP accelerated phase, BC blast crisis. c 32DMIGIR and 32DBCR−ABL cells were collected, and the indicated proteins were examined by western blot. d, e Protein (d) and mRNA (e) levels of USP47 in BCR-ABL stably knocked down K562 cells (Sh BCR-ABL) and vector-transfected cells (Ctrl ShRNA) (n = 3 biologically independent samples per group). Data are presented as mean ± s.d. ***p < 0.001, using two-sided Student’s t-test. f K562 cells were treated with IM for 24 h, and the indicated proteins were examined by western blot. g STAT5 knockdown decreased USP47 expression in the K562 cells. h Pan-RAS-IN-1 (RAS inhibitor) and U0126 (ERK inhibitor) decreased USP47 expression in the K562 cells after 24 h of treatment. Source data are provided as a Source Data file.