Hua Bai

The paper identifies SCAF1 as a key mediator of peroxisome-to-mitochondria signaling under import stress, showing its role in suppressing mitoribosome biogenesis and driving cellular senescence.

The paper shows that peroxisomal protein import in Drosophila cortex glia is circadian and affects sleep and lipid metabolism, with Pex5 playing a key role.

This study develops OptoMitoTether, an optogenetic system to control mitochondrial proximity, which increases membrane potential and reduces blue light-induced damage in cells and C. elegans.

The paper identifies FATP2 as a conserved target for preventing starvation-induced liver atrophy by reducing fatty acid uptake in cavefish and other species.

The paper identifies acetyl-CoA-mediated autoacetylation of FASN at K813 as a regulatory mechanism for de novo lipogenesis in Drosophila larvae.

The paper shows a lncRNA interacts with β-Spectrin to regulate spermatogenesis and endosomal processes in Drosophila fat bodies.

This study shows FOXO maintains neuromuscular junction integrity during aging in Drosophila by repressing MAPK signaling.

This study shows that mTORC2 protects Drosophila hearts from HFD-induced mitochondrial and cardiac dysfunction by maintaining mitochondrial homeostasis.

This study shows that peroxisome import stress reduces ribosome biogenesis and activates the integrative stress response through eIF2α phosphorylation in both Drosophila and human cells.

This study investigates age-related changes in FOXO transcription factor gene targeting in Drosophila melanogaster using ChIP-Seq, revealing a decline in FOXO-bound genes and shifts in targeted biological processes with age.

This study uses RiboTag sequencing to analyze the translatome of Drosophila oenocytes under aging and oxidative stress, identifying shared molecular mechanisms with mammalian liver aging.

This study shows activin signaling negatively regulates cardiac autophagy and health during aging in Drosophila, with mTORC2 playing a key role.

This study identifies a physical and genetic interaction between dFOXO and Kr-h1 in Drosophila, showing that Kr-h1 represses lipolysis by regulating adipose lipase brummer transcription.