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Figure 2a/b/h/j. Phosphatase activity and substrate recognition features of the different DLAR constructs.

Figure 4. Evaluation of the phosphotyrosine binding pocket of the PTP domains of DLAR and PTP99A using para-

Nitrocatecholsulphate (PNC).

Figure 5. Inter-domain interactions and inter-atomic networks for the PTP domains obtained from molecular dynamics simulations.

Figure 1. Interaction of MU2 and HP1a.

Figure 3. Effects of HP1a depletion on focal movement.

Figure 4. HP1a is not recruited to IRIF and laser induced breaks.

Figure 5. MU2 and cH2Av recognize stalled replication forks.

Fig 7. Treatment of S2 cells with HP1a dsRNA leads to a decrease in the number of cells in S phase and an apparent increase in the number of cells at both G1 and G2/M.

Figure 7. HP1a depletion affects cell cycle in S2 cells.

Figure 8. Apoptosis and G2/M checkpoint in wing discs.

Figure 2. Subcellular localization of FUS in prostate cancer cells

Figure 1 establishes that FUS is complexed with AR. Figure 3 demonstrates that FUS possesses innate ability to regulate transcription. Figure 4 demonstrates that FUS modulates AR activity.

Figure 1

Figure 2. PolyQ-length-dependent interaction between HAP1 and AR.

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fig 2C: we found that the C27–C64 disulfide was formed in the presence of Mia40-WT. Of importance, in the absence of functional Mia40 no oxidation of the two cysteines occurred