LRRK2 kinase inhibition restores haloperidol effects on rpS6 signaling in iSPNs

Output Details

Previous studies have shown that the phosphorylation of ribosomal protein S6 (p-rpS6) at S235/236 residues increases in iSPNs in response to haloperidol activation. This phosphorylation is cAMP/PKA dependent, which is the canonical pathway inhibited by D2R antagonism. We therefore explored whether LRRK2 inhibition interferes with this haloperidol-mediated phosphorylation event.

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Aligning Science Across Parkinson's
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