Nicole L. Stuhr

This study identifies molecular mechanisms by which C. elegans avoid Methylobacterium after ingestion, integrating lipid metabolism and dietary needs to influence food preference.

The paper identifies reductive stress as a toxicity of biguanides like metformin, showing that fatty acid biosynthesis protects against this effect and could be targeted in cancer.

This study identifies that impaired ribosomal RNA biogenesis enhances resistance to reductive stress in C. elegans by reducing NADPH/NADH accumulation and GSH levels.

The paper shows that constitutive SKN-1 activation in C. elegans leads to serotonin deficiency, causing apathy toward pathogens and reduced survival.

The paper identifies drh-1 as a mechanism to counteract excessive SKN-1 transcriptional activity in C. elegans, improving healthspan by opposing age-related pathology.

This study identifies ether lipid biosynthesis as a key pathway mediating the longevity benefits of biguanides like metformin in C. elegans.

This study shows that riboflavin depletion in C. elegans extends lifespan and improves metabolic health through multiple pathways.

The paper identifies ALDH4A1 genetic variation as a biomarker for age-related muscle health across species using C. elegans and human data.