Douglas C. Wallace

This paper introduces mtMagLOV2, a quantum sensor that measures mitochondrial redox state via magneto-fluorescence, distinguishing between cancer and cardiomyocytes.

nAPOGEE assesses pathogenicity of mitochondrial noncoding variants using machine learning, revealing consistent spatial correlation of predicted pathogenicity.

This study shows that mitochondrial DNA mutations in NSCLC cause respiration defects, leading to glucose dependency, reduced serine synthesis, and increased cancer survival.

This study identifies mitochondrial hyperactivity and reactive oxygen species as critical drivers of innate immunity to the YFV-17D vaccine, enhancing IFN response and vaccine effectiveness.

This study identifies ZNFX1 as a master regulator of epigenetically-induced pathogen mimicry and inflammasome signaling in ovarian cancer, linking its expression to disease progression and survival.

The paper shows low magnetic fields increase mitochondrial respiration and decrease reactive oxygen species in rat heart mitochondria, with a bell-shaped response, possibly via a radical pair mechanism.

This study identifies non-canonical genes linked to RAAS overactivation in lethal COVID-19, causing multi-organ damage and mediastinal lymph node dysfunction.

The paper shows that N1-methylation at position 9 of mt-Leu(UAA) stabilizes wild-type mt-tRNA but destabilizes pathogenic variants, suggesting methylation control could be therapeutic.

The paper analyzes optical mapping data from Black and white genomes to reveal structural differences in 22q11.2 low copy repeats (LCR22s) and their potential role in the lower prevalence of 22q11.2DS in Black individuals.

APOGEE 2 improves pathogenicity prediction for mitochondrial missense variants using a machine learning model based on ACMG/AMP guidelines and provides region-wise genome fragility assessments.

The paper identifies a lncRNA signature associated with SARS-CoV-2 infection through transcriptomic analysis and functional correlation studies.

The paper identifies a mitochondrial haplogroup mutation interacting with a HDC variant to cause mitochondrial dysfunction and connective tissue disorder.

This study investigates how SARS-CoV-2 infection affects mitochondrial gene expression in different tissues and disease stages, finding targeted inhibition in some organs and upregulation in others.

The paper identifies miR-2392 as a miRNA involved in SARS-CoV-2 infection, showing its role in inflammation, glycolysis, and hypoxia, and develops a miRNA-based therapeutic targeting it.