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JNK3 MEDIATED STRESS SIGNALLING IS AN EARLY PLAYER IN ROTENONE-INDUCED NEURODEGENERATION
Muhammad Saifand 4 co-authors
Aston University
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS03-08AM-073
Presentation
Date TBA
Board: PS03-08AM-073
Event Information
Poster Board
PS03-08AM-073
Poster
View posterAbstract
Parkinson’s disease is the second most common neurodegenerative disorder, yet the early signalling mechanism remains poorly understood. In this study, we show that c-Jun N-terminal kinase 3 (JNK3), a stress-activated protein kinase primarily expressed in the central nervous system, is a key-player in the early events triggered by a Parkinsonian toxin. Using differentiated SH-SY5Y neuroblastoma cells and KOLF2.1J human induced pluripotent stem cell–derived neurons, we show that exposure to rotenone, a mitochondrial complex I inhibitor, induces progressive neuronal cell death. Rotenone treatment is accompanied by rhythmic fluctuations in JNK3 expression in both cellular models. Time-resolved analyses reveal that JNK3 expression oscillates in a striking anti-phase manner between SH-SY5Y and iPSC-derived neurons (Pearson r = −0.866), such that peak expression in one model coincides with minimal expression in the other. These findings suggest that rhythmic JNK3 signalling represents a conserved cellular response to mitochondrial stress, with dynamics that are strongly dependent on cell identity, and identifies JNK3 as a critical contributor to selective neuronal vulnerability in Parkinson’s disease.
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