Figure 1. Models for RMS HSP70 dependence. Top, the RMS ER carries a specific HSP70 client that misfolds after treatment, activating the UPR. Client-expressing tumors are sensitive to HSP70 inhibition. Below, the RMS UPR is “primed” at rest and slight perturbation by HSP70 inhibition reaches apoptotic threshold. HSP70 inhibitors are predicted to be most effective in cells with high resting UPR sensitivity.
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