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18) suggests that the AR + BCL-2 + phenotype in VCaP-AD is likely driven by GR signaling whereas the AR cyto BCL-2 -/lo phenotype in VCaP-AI is most plausibly engendered by ARv7 with contributions from the AR-FL (supplementary Fig

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If the cellular clearance rate of misfolded SOD1 is inadequate, increasingly frequent hydrophobic interactions ultimately give way to aggregation, forming larger amorphous structures that stress the cellular machinery 21