Prolonged Nuclear Retention of Activated Extracellular Signal-regulated Protein Kinase Promotes Cell Death Generated by Oxidative Toxicity or Proteasome Inhibition in a Neuronal Cell Line
Open Access
- 1 February 2002
- journal article
- Published by Elsevier BV in Journal of Biological Chemistry
- Vol. 277 (6), 4010-4017
- https://doi.org/10.1074/jbc.m104479200
Abstract
No abstract availableKeywords
This publication has 66 references indexed in Scilit:
- Signaling Complexes and Protein-Protein Interactions Involved in the Activation of the Ras and Phosphatidylinositol 3-Kinase Pathways by the c-Ret Receptor Tyrosine KinaseJournal of Biological Chemistry, 2000
- Stress‐mediated inhibition of the classical nuclear protein import pathway and nuclear accumulation of the small GTPase Gsp1pThe FASEB Journal, 2000
- Significance of Nuclear Relocalization of ERK1/2 in Reactivation of c-fos Transcription and DNA Synthesis in Senescent FibroblastsJournal of Biological Chemistry, 2000
- ERK1b, a 46-kDa ERK Isoform That Is Differentially Regulated by MEKJournal of Biological Chemistry, 2000
- Oxidative Stress Triggers STAT3 Tyrosine Phosphorylation and Nuclear Translocation in Human LymphocytesJournal of Biological Chemistry, 1999
- A Novel Regulatory Mechanism in the Mitogen-activated Protein (MAP) Kinase CascadeJournal of Biological Chemistry, 1997
- Opposing Effects of ERK and JNK-p38 MAP Kinases on ApoptosisScience, 1995
- How MAP Kinases Are RegulatedJournal of Biological Chemistry, 1995
- Activation of MAP kinase kinase is necessary and sufficient for PC12 differentiation and for transformation of NIH 3T3 cellsCell, 1994
- ERKs: A family of protein-serine/threonine kinases that are activated and tyrosine phosphorylated in response to insulin and NGFCell, 1991