Timothy E. Shutt

This study shows that activating the AhR in TRPV1+ nociceptors reduces visceral hypersensitivity in post-colitis mice, suggesting AhR as a therapeutic target for IBD-related abdominal pain.

This study shows that mitochondrial proteostasis stress causes a biphasic cortisol response, with mild stress increasing and severe stress decreasing cortisol production, linking mitochondrial function to steroidogenesis in Parkinson's disease models.

The paper identifies how pathogenic MFN2 variants cause mtDNA release into endosomes and mitochondrial-derived vesicles, triggering inflammation and myopathy, and suggests a therapeutic strategy using integrated stress response activation.

The paper identifies ataxia-linked MFN2 variants that increase ferroptosis susceptibility by enhancing fatty acid import from lipid droplets to mitochondria, leading to lipid peroxidation and cell death.

The paper identifies two compounds that activate the HRI pathway, improving mitochondrial function in MFN2-deficient cells.

The paper identifies a novel MFN2 variant, Q367H, linked to mtDNA-mediated inflammation in a patient with distal myopathy, revealing a pathomechanism connecting MFN2 dysfunction to inflammatory signaling.

The paper validates the genus Pocheina by showing that its SSU rRNA sequence was contaminated, leading to the recognition of three major lineages in Acrasidae.

This paper describes a modified viral transduction method to differentiate iPSCs into steroidogenic cells by first forming embryoid bodies before SF1 transduction.

This study shows that pharmacologic activation of ISR kinases HRI or GCN2 prevents mitochondrial fragmentation in disease models.

The paper identifies a novel homozygous MFN2 variant R334K linked to a lethal neonatal disorder and shows it causes severe mitochondrial dysfunction, confirmed through functional studies and Drosophila modeling.

The paper shows that most axonal mitochondria in mammalian neurons lack mtDNA and do not produce ATP, contrasting with dendritic mitochondria.

The paper describes a protocol to measure mtDNA synthesis, turnover, and supercoiling using selective bromodeoxyuridine incorporation and Southwestern blotting.

This study shows that reactive oxygen species (ROS) mediate the pro-adipogenic effects of bisphenol A and its analogues by enhancing adipogenesis through mitochondrial ROS production.

The paper reports a novel MFN2 variant associated with ataxia, optic atrophy, and sensorineural hearing loss, and shows its functional impact in patient fibroblasts.

The paper characterizes two TOP1MT variants in a patient with hypertrophic cardiomyopathy, showing both impair mitochondrial functions but affect different aspects of mtDNA regulation.

The paper identifies PISD as a mitochondrial disease gene causing skeletal dysplasia, cataracts, and white matter changes through exome sequencing and functional analysis of patient fibroblasts.