c-Jun N-terminal Kinase (JNK)-dependent Acute Liver Injury from Acetaminophen or Tumor Necrosis Factor (TNF) Requires Mitochondrial Sab Protein Expression in Mice
作者： Sanda Win , Tin Aung Than , Derick Han , Lydia M. Petrovic , Neil Kaplowitz
关键词: Bruton's tyrosine kinase 、 Serine threonine protein kinase 、 Signal transduction 、 Cell biology 、 MAPK/ERK pathway 、 c-jun 、 Liver injury 、 Kinase 、 Biology 、 Mitochondrion
摘要: Sustained JNK activation plays a critical role in hepatotoxicity by acetaminophen or GalN/TNF-α. To address the importance of translocation to mitochondria that accompanies sustained these models, we assessed expression potential initial target outer membrane mitochondria, namely Sab (SH3 domain-binding protein preferentially associates with Btk), also known as Sh3bp5 5). Silencing liver using adenoviral shRNA inhibited and mitochondrial targeting upstream MKK4 (MAPK kinase 4), accompanied striking protection against injury vivo cultured hepatocytes both toxicity models. We conclude may serve platform for MAPK pathway enzymes interaction stress-activated is required toxicity.
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