Viktor I. Korolchuk

The paper identifies SQ-1 as a small molecule that activates autophagy by promoting p62 oligomerisation, improving mitochondrial clearance and cell viability in NPC1 disease models.

This study shows that AMPK senses NAD levels, with NAD binding to the gamma subunit and modulating AMPK activity, which affects metabolic pathways like mTORC1 and autophagy.

This study shows that ubiquilin-2 droplets catalyze α-synuclein fibril formation in vitro and in cells, and identifies a compound that inhibits this process.

This study identifies nitro-oleic acid (OA-NO2) as a compound that re-sensitizes PARPi-resistant TNBC cells to PARPi by targeting p62 and inhibiting autophagy.

This study shows that developmental mitochondrial complex I dysfunction reduces lifespan and stress resistance, while adult-onset dysfunction increases lifespan and stress resistance.

The paper uses single-cell analyses to show that oncogenic PIK3CAH1047R reduces IGF1 signaling specificity and enhances EGF responses, leading to increased phenotypic heterogeneity.

The paper investigates whether Lewy bodies form due to impaired autophagy and mitochondrial dysfunction, finding enriched autophagic markers and proteomic evidence of aggresome-like pathways in Lewy bodies.

This study identifies inflammation and autophagy dysfunction, linked to mTOR pathway activation, as key mechanisms in metachromatic leukodystrophy using postmortem tissue analysis.

This study shows that developmental mitochondrial dysfunction limits lifespan in Drosophila, while adult dysfunction accelerates ageing, with metabolic adaptations during development being critical for survival.