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Misguided Transcriptional Elongation Causes Mixed Lineage Leukemia

Figure 1

Core structure of the EAP complex.

Schematic representation of the EAP core and stabilizing protein interactions. The composition of the EAP core, protein interaction motifs, and the enzymatic reactions catalyzed by EAP are depicted. Please note the individual protein orientation with N- and C-termini labeled appropriately. For clarity, only one RNA Pol II repeat sequence (YSPTSPS) is shown. Solid lines mark protein–protein interaction domains. The exact N-terminal extent of the CyclinT2 binding site in Dot1l could not be delineated, and therefore, this boundary is represented by a dashed line. The interaction of histone H3 with the YEATS domain of ENL has been described previously [20]. The calculated molecular weights from the respective reference sequences are given for each protein. Numbers denote the respective amino acid residues of the individual interaction domains. Abbreviations are used as follows: AF4, ALL1 fused gene on Chromosome 4 (also known as MLLT1 or AFF1); ALF, AF4-LAF4-FMR2 homology region; CDK9, cyclin dependent kinase 9; CHD, C-terminal homology domain; cyc box, cyclin box; CYCT, Cyclin T2; H, histidine rich; Dot1l, disruptor of telomeric silencing like; ENL, eleven nineteen leukemia; H3, histone H3; H3K79met, Histone H3 Lysine 79 methyltransferase domain; hydp, hydrophobic region; L, leucine rich; KRM, lysine-arginine-rich motif; NHD, N-terminal homology domain; NLS, nuclear localization signal; P, proline rich region; Ser, serine rich domain; YEATS, Yaf9, ENL, AF9, Taf14, and Sas5 conserved domain.

Figure 1

doi: https://doi.org/10.1371/journal.pbio.1000249.g001