Figure 1.
Schematics depicting the functional domains and breakpoints for ABL1 and ABL2 fusion genes. In all fusion genes, the ABL1 (A) and ABL2 (B) tyrosine kinase domains are retained and the autoinhibitory myristate moieties are truncated. The residues required for formation of the myristate binding pocket are retained in all fusions as indicated by black triangles above the kinase domain. Fusion of different 5’ partner genes results in retention (breakpoint at exon 2), truncation (breakpoint at exon 3), or deletion (breakpoint at exon 4) of the ABL1/ABL2 SH3 domain. Breakpoints are denoted by vertical bold black lines and exons by vertical dashed lines. Diagonal dashed lines indicate unstructured regions of fusion partner genes that have been omitted for simplicity. The following isoforms were used for schematic construction: ABL1 NM_007313 and ABL2 NM_001168238.

Schematics depicting the functional domains and breakpoints for ABL1 and ABL2 fusion genes. In all fusion genes, the ABL1 (A) and ABL2 (B) tyrosine kinase domains are retained and the autoinhibitory myristate moieties are truncated. The residues required for formation of the myristate binding pocket are retained in all fusions as indicated by black triangles above the kinase domain. Fusion of different 5’ partner genes results in retention (breakpoint at exon 2), truncation (breakpoint at exon 3), or deletion (breakpoint at exon 4) of the ABL1/ABL2 SH3 domain. Breakpoints are denoted by vertical bold black lines and exons by vertical dashed lines. Diagonal dashed lines indicate unstructured regions of fusion partner genes that have been omitted for simplicity. The following isoforms were used for schematic construction: ABL1 NM_007313 and ABL2 NM_001168238.

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