Abstract:<p>S1: LBD-ER mutations are expressed at physiologic levels and are E2-independent. S2: LBD-ER lead to an enrichment pathway of ECM degradation S3: High concentrations of E2 do not recapitulate the mutant phenotype in WT-ER expressing cells. S4: LBD-mutations activate the AKT/mTOR pathway. S5: Mitochondrial activity of D538G-ER expressing T47D cells. S6: Glutamine leads to enrichment of specific pathways by 537S-ER.</p>
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