Fig. 3: Feedback regulation between DYRK1A and MYC in KMT2A-R ALL. | Leukemia

Fig. 3: Feedback regulation between DYRK1A and MYC in KMT2A-R ALL.

From: DYRK1A inhibition results in MYC and ERK activation rendering KMT2A-R acute lymphoblastic leukemia cells sensitive to BCL2 inhibition

Fig. 3

A Phophoproteomics analysis in HB11;19 cells treated with 5 µM GNF2133 for 2 h and 8 h. B Western blot analysis of MYC and β-actin in KMT2A-R ALL cell lines treated either with control or EHT1610 (5 µM/72 h). C Dyrk1a gene expression levels in a comprehensive panel of purified developmentally defined normal murine B cells and genetically distinct murine lymphoma models (GSE26408) [40]. D Chip-Seq experiment on the MYC-inducible B cell malignancy model cell line P493-6. Gene tracks of Myc binding at the Dyrk1a promoter region at 0 h (top), 1 h (middle), and 24 h (bottom) are shown (GSE36354) [43]. E Myc and Dyrk1a gene expression levels in P493-6 cells before and after MYC inactivation. Myc inactivation was induced via tetracycline treatment for 48 h (GSE120246). F Myc and Dyrk1a gene expression levels in Eμ-myc transgenic mice. Data are represented as individual values with mean ± SEM bars. *P < 0.05; **P < 0.01; ***P < 0.001 by t-test.

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