D. J. Pagliarini

This study identifies COQ4 as catalyzing the oxidative decarboxylation of the C1 carbon in CoQ biosynthesis in eukaryotic cells.

The paper shows CoQ4 can substitute for CoQ10 in cells and describes mitochondrial-targeting compounds that deliver CoQ4.

This study shows that statin-induced downregulation of TOMM40 and TOMM22 disrupts mitochondrial dynamics, morphology, and mitophagy in skeletal myotubes, and overexpression of these genes rescues these effects.

The paper identifies Hem25p as a mitochondrial IPP transporter in yeast, essential for CoQ biosynthesis.

This study shows that Pptc7 maintains mitochondrial protein content by suppressing receptor-mediated mitophagy, leading to metabolic defects and early lethality in mice.

The paper identifies Aim18p and Aim46p as mitochondrial hemoproteins in yeast with structural similarities to CHI proteins but distinct functional roles.

The paper presents the structure and functional analysis of a multimeric COQ7:COQ9 complex involved in CoQ biosynthesis, revealing its mechanism for accessing hydrophobic precursors and coordinating CoQ synthesis.

The paper develops small molecule inhibitors and activators for COQ8A, a UbiB family protein, using crystallography, NMR, and mass spectrometry to modulate its function in CoQ biosynthesis.

This study identifies two mitochondrial proteins, Cqd1 and Cqd2, that regulate CoQ distribution and oxidative stress resistance in yeast.

This paper develops a label-free method using NAD(P)H and FAD autofluorescence imaging and machine learning to classify T cell activation states and subtypes with high accuracy.

This study shows that Pptc7 is essential for mitochondrial metabolism and biogenesis, as its deletion in mice causes metabolic defects and early death.

This study identifies Puf3p as a regulator of CoQ biosynthesis through transomic analysis, revealing its role in controlling Coq5p levels and mitochondrial biogenesis.