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We found that wild-type (WT) ACTL6A and the DNBL, CC, and NBC ACTL6A mutants reversed the inhibition of cell proliferation and the reduced GCLC protein expression induced by knocking down ACTL6A expression, but the ACTL6A HR-deleted mutant did not show this restorative effect (Fig
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NMDA receptor channels: subunit-specific potentiation by reducing agents
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