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. 2015 Jan 21;14(7):973–979. doi: 10.1080/15384101.2015.1006970

Figure 2.

Figure 2.

BCR-ABL promotes PTEN inactivation through Casein Kinase II. (A) PTEN-phosphorylation in parental and BCR-ABL-NIH3T3 treated with 1 μM imatinib and 60 μM TBB for 10 hours. To obtain a comparable level of expression of PTEN, the amount of BCR-ABL-NIH3T3 extracts were increased of 20% compared to parental NIH3T3 cells. (B) Schematic representation of PTEN with the indication of PTEN tail phosphorylation sites. (C) Co-immunoprecipitation of CKII-α and p210-BCR-ABL in BCR-ABL-infected NIH3T3 cells. (D) In vitro kinase assay with immunoprecipitated PTEN and CKII-α and purified ABL kinase. One μM Imatinib was added to the in vitro reaction for 10 minutes. Phospho-PTEN: Phospho-S380/T382/T383; P-Tyr: Phospho-Tyrosine: the band corresponds to the BCR-ABL molecular weight. (E) Transient transfection of Myc-PTEN mutants in BCR-ABL-infected NIH3T3 cells. 48 hours after transfection, myc-tag immunofluorescence was performed to verify PTEN compartmentalization. PTEN-TM: PTEN-S380A/T382A/T383A.