Hanlin Zhang

This study shows that E. faecalis activates the UPRMT in C. elegans through metabolic and oxidative stress, not direct mitochondrial damage.

This study shows that aging reduces 2,6-linked sialic acids on T cells, leading to exhaustion and impaired immune function.

This study shows that macroautophagy-induced lysosomal damage limits quiescent cell re-entry, and reducing this damage can enhance cell cycle re-entry in C. elegans and mammalian cells.

The paper shows that germline mitochondria mediate neuron-to-peripheral UPRMT signaling in C. elegans by responding to mitokines like WNT and serotonin and regulating lipid metabolic pathways.

This study shows that the olfactory nervous system in C. elegans regulates mitochondrial function and stress responses through mitophagy and the UPRMT pathway.

This study identifies SKN-1 as a metabolic surveillance factor that responds to amino acid catabolism to influence stress resistance in C. elegans.