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Figure 1.

AML sample list and RNAseq data collection.

A. A total of 45 AML samples were used for the analysis, including 29 normal karyotype AML, 8 abnormal karyotype AML and 8 AML without karyotype information. B. RNAseq data collected from the 45 AML cases.

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Figure 2.

Fusion transcript information.

A. Fusion transcripts identified in different types of AML. B. Validated fusion transcripts identified in normal karyotype AML.

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Figure 3.

NFATC3-PLA2G15 fusion.

The fusion is formed between upstream gene NFATC3 and downstream gene PLA2G15 in 3′-5′ tail to head orientation. In this fusion, amino acid V (GTC) is shared at the fusion point (G from NFATC3 and TC from PLA2G15). A. Wild-type NFATC3 protein sequence; B. Wild-type PLA2G15 protein sequence; C. NFATC3-PLA2G15 fusion protein sequences. The bold V residue marks the fusion junction.

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Figure 4.

Validation of sense and antisense fusion transcripts by strand-specific RT-PCR.

A. Summary for RNA samples from 8 myeloid cell lines. B. CIITA-DEXI sense and antisense fusion transcripts detected in myeloid cell lines and AML samples. +: positive control with beta-actin; -: netative control without RNA templates.

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Figure 5.

Long-range PCR results.

A. Summary of the results from 11 fusion candidates. B. Size distribution of the amplified genomic DNA fragments.

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Figure 6.

CIITA-DEXI fusion.

A. CIITA-involved protein-protein interaction network. B. Mapping and validation of CIITA-DEXI fusion. Three CIITA-DEXI fusions were detected. In the fusion, CIITA preserved the coding exone till the stop codon but losed its 3′ untranslated region. This fusion was detected by 23 paired-end RNAseq sequences and validated by Sanger sequencing.

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