Figure 8.
Figure 8. Inhibition of NPM-ALK–mediated IL3-independent proliferation of Ba/F3 cells by disruption of NPM-ALK Src-kinase interaction. (A) The expression level of wild-type NPM-ALK (Ba/F3 N/A) or the NPM-ALK Y418F mutant Ba/F3 (clones 1, 2) was detected by immunoblotting with the ALKc antibody. (B) Of each clone, 10 million cells were subjected to immunoprecipitation with the Src-2 antibody followed by immunoblotting with ALKc. (C) Clones expressing wild-type NPM-ALK or the Y418F NPM-ALK mutant were plated at 103 cells per well in a 96-well plate in medium starved of IL3. Proliferation of the different clones was determined each day for 6 days using an MTT proliferation assay. Results are means of triplicates ± SEM of 1 experiment representative of 3.

Inhibition of NPM-ALK–mediated IL3-independent proliferation of Ba/F3 cells by disruption of NPM-ALK Src-kinase interaction. (A) The expression level of wild-type NPM-ALK (Ba/F3 N/A) or the NPM-ALK Y418F mutant Ba/F3 (clones 1, 2) was detected by immunoblotting with the ALKc antibody. (B) Of each clone, 10 million cells were subjected to immunoprecipitation with the Src-2 antibody followed by immunoblotting with ALKc. (C) Clones expressing wild-type NPM-ALK or the Y418F NPM-ALK mutant were plated at 103 cells per well in a 96-well plate in medium starved of IL3. Proliferation of the different clones was determined each day for 6 days using an MTT proliferation assay. Results are means of triplicates ± SEM of 1 experiment representative of 3.

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