Figure 2
Figure 2. Clonal expansion of PML-B2 and RARA-LBD mutations during disease progression. (A) Schematic representation of PML, RARA, and its fusion proteins with or without mutations. Functional domains are indicated. Gray arrowheads indicate the break points of the fusion proteins. Black asterisks depict amino acid substitutions resulting from genetic mutations. Black arrows indicate the positions of the PCR primers for amplifying PML-RARA fusion transcripts. RING indicates the RING finger; B1 and B2, B-box motifs; C-C, coiled-coil; and DBD, DNA-binding domain. (B) Clonal expansion of PML-RARA mutants. Using the clinical samples obtained at time points 1-5 in Figure 1A, RT-PCR using PCR primers (PML-U and RARA-L in Figure 1A) followed by cloning was performed. At least 20 clones were sequenced for each sample. The percentages of the clones are depicted in the bar graph.

Clonal expansion of PML-B2 and RARA-LBD mutations during disease progression. (A) Schematic representation of PML, RARA, and its fusion proteins with or without mutations. Functional domains are indicated. Gray arrowheads indicate the break points of the fusion proteins. Black asterisks depict amino acid substitutions resulting from genetic mutations. Black arrows indicate the positions of the PCR primers for amplifying PML-RARA fusion transcripts. RING indicates the RING finger; B1 and B2, B-box motifs; C-C, coiled-coil; and DBD, DNA-binding domain. (B) Clonal expansion of PML-RARA mutants. Using the clinical samples obtained at time points 1-5 in Figure 1A, RT-PCR using PCR primers (PML-U and RARA-L in Figure 1A) followed by cloning was performed. At least 20 clones were sequenced for each sample. The percentages of the clones are depicted in the bar graph.

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