SP600125, a selective JNK inhibitor, protects ischemic renal injury via suppressing the extrinsic pathways of apoptosis
- 1 May 2007
- journal article
- Published by Elsevier in Life Sciences
- Vol. 80 (22) , 2067-2075
- https://doi.org/10.1016/j.lfs.2007.03.010
Abstract
No abstract availableKeywords
This publication has 28 references indexed in Scilit:
- Apoptosis: a basic biological phenomenon with wide‐ranging implications in human diseaseJournal of Internal Medicine, 2005
- Regulation and interplay of apoptotic and non‐apoptotic cell deathThe Journal of Pathology, 2005
- Testosterone Is Responsible for Enhanced Susceptibility of Males to Ischemic Renal InjuryJournal of Biological Chemistry, 2004
- Effect of an inhibitor of Jun N‐terminal protein kinase, SP600125, in single allergen challenge in sensitized ratsImmunology, 2004
- Apoptosis and JNK activation are differentially regulated by Fas expression level in renal tubular epithelial cellsKidney International, 2001
- Death Receptors: Signaling and ModulationScience, 1998
- Mitochondria and ApoptosisScience, 1998
- Requirement for ceramide-initiated SAPK/JNK signalling in stress-induced apoptosisNature, 1996
- Opposing Effects of ERK and JNK-p38 MAP Kinases on ApoptosisScience, 1995
- Phosphorylation of c-jun mediated by MAP kinasesNature, 1991