Costin N. Antonescu

Mitophagy is required for cell survival upon ultrasound and microbubble therapeutic exposure

This study shows that mitophagy is essential for cell survival after ultrasound and microbubble treatment by mitigating mitochondrial damage and metabolic stress.

Pathogenic Mitofusin 2 variants causing myopathy drive endosomal mtDNA release and inflammation

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.

Spatially localized ligand binding to receptors affects magnitude and timing of signaling response

The paper models how spatially localized ligand binding to receptors affects signaling response consistency, ligand requirements, and response timing compared to uniform binding.

AMPK Repositions Early Endosomes via Gapex-5 to Promote Delivery of Iron to Mitochondria

This study shows AMPK moves early endosomes to mitochondria via Gapex-5 to enhance iron delivery under nutrient scarcity.

Differences in intrinsic cellular O-GlcNAcylation impact response to metabolic stress

This study investigates how intrinsic levels of O-GlcNAcylation affect the response to metabolic stress and the orthogonality of AMPK and O-GlcNAc signaling pathways.

NCK adaptor proteins regulate clathrin-coated pit dynamics and EGF-stimulated PI3K-Akt signaling

This study shows Nck adaptor proteins regulate clathrin-coated pit dynamics and EGF-stimulated PI3K-Akt signaling, affecting cell proliferation and survival.

Cargo-selective regulation of clathrin-mediated endocytosis by AMP-activated protein kinase

This study shows AMPK regulates clathrin-mediated endocytosis by controlling Dab2 and Arf6 to selectively internalize β1-integrin.

Control of GSK3beta nuclear localization by amino acid signaling requires GATOR1 but is mTORC1 independent

The paper shows that GATOR1 regulates GSK3β nuclear localization in response to amino acids, independent of mTORC1, and that this process supports cell survival under metabolic stress.