10.1016/S0009-9120(87)80090-5
c-Jun N-terminal kinase mediates mouse liver injury through a novel SAB (SH3BP5)-dependent pathway leading to inactivation of intramitochondrial Src
It was originally designed as a potential investigational treatment for neurodegenerative conditions, particularly Alzheimers disease
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This discovery reveals previously unrecognized anti-inflammatory mechanisms of HSC, suggesting that its therapeutic strategy involving TLR4 modulation for AKI diverges from conventional clinical approaches such as dialysis and antibiotic therapies
