ro 31-8425 and Necrosis

ro 31-8425 has been researched along with Necrosis in 1 studies

Research

Studies (1)

Timeframe	Studies, this research(%)	All Research%
pre-1990	0 (0.00)	18.7374
1990's	0 (0.00)	18.2507
2000's	0 (0.00)	29.6817
2010's	1 (100.00)	24.3611
2020's	0 (0.00)	2.80

Authors

Authors	Studies
Gaarde, WA; Han, D; Johnson, HS; Kaplowitz, N; Saberi, B; Ybanez, MD	1

Other Studies

1 other study(ies) available for ro 31-8425 and Necrosis

Article	Year
Protein kinase C (PKC) participates in acetaminophen hepatotoxicity through c-jun-N-terminal kinase (JNK)-dependent and -independent signaling pathways. Hepatology (Baltimore, Md.), 2014, Volume: 59, Issue:4 Topics: Acetaminophen; AMP-Activated Protein Kinases; Animals; Cells, Cultured; Chemical and Drug Induced Liver Injury; Disease Models, Animal; Hepatocytes; In Vitro Techniques; Indoles; JNK Mitogen-Activated Protein Kinases; Male; Maleimides; Mice; Mice, Inbred C57BL; Mitochondria, Liver; Necrosis; Protein Kinase C; Protein Kinase Inhibitors; Signal Transduction	2014

Article

Year

Protein kinase C (PKC) participates in acetaminophen hepatotoxicity through c-jun-N-terminal kinase (JNK)-dependent and -independent signaling pathways.

Hepatology (Baltimore, Md.), 2014, Volume: 59, Issue:4

Topics: Acetaminophen; AMP-Activated Protein Kinases; Animals; Cells, Cultured; Chemical and Drug Induced Liver Injury; Disease Models, Animal; Hepatocytes; In Vitro Techniques; Indoles; JNK Mitogen-Activated Protein Kinases; Male; Maleimides; Mice; Mice, Inbred C57BL; Mitochondria, Liver; Necrosis; Protein Kinase C; Protein Kinase Inhibitors; Signal Transduction

2014