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Inactivation of bad by site-specific phosphorylation: the checkpoint for ischemic astrocytes to initiate or resist apoptosis
- Source :
- Journal of neuroscience research. 79(6)
- Publication Year :
- 2005
-
Abstract
- Bcl-2-associated death protein (Bad), a member of the Bcl family, directs astrocytes in primary cultures to enter or resist apoptosis during ischemia in vitro. Under ischemia, Bad was the only Bcl family member whose expression was upregulated significantly during the early stages of an ischemic insult. Increased endogenous Bad was translocated from the cytoplasm to mitochondria to induce apoptosis in astrocytes. Concurrently, ischemia also induced Bad phosphorylation specifically on Ser112 to promote survival. This site-specific phosphorylation of Bad was mediated by an early activation of the mitogen-activated protein kinase/extracellular signal-regulated protein kinase (MAPK/ERK) intracellular signaling pathway. This study demonstrates that ischemia-induced Bad plays a dual role in determining whether astrocytes enter or resist apoptosis after an ischemic insult. © 2005 Wiley-Liss, Inc.
- Subjects :
- MAPK/ERK pathway
Time Factors
Blotting, Western
Green Fluorescent Proteins
Ischemia
Apoptosis
Biology
Transfection
Models, Biological
Cellular and Molecular Neuroscience
chemistry.chemical_compound
Mice
Phosphatidylinositol 3-Kinases
Downregulation and upregulation
medicine
In Situ Nick-End Labeling
Animals
Immunoprecipitation
LY294002
Phosphorylation
Protein kinase A
Cells, Cultured
Fluorescent Dyes
Cerebral Cortex
Mitogen-Activated Protein Kinase Kinases
Neurons
Mice, Inbred ICR
Cytochromes c
medicine.disease
Immunohistochemistry
Cell biology
Mitochondria
medicine.anatomical_structure
chemistry
Animals, Newborn
Gene Expression Regulation
Astrocytes
Enzyme Induction
Mutagenesis, Site-Directed
bcl-Associated Death Protein
Carrier Proteins
Astrocyte
Subjects
Details
- ISSN :
- 03604012
- Volume :
- 79
- Issue :
- 6
- Database :
- OpenAIRE
- Journal :
- Journal of neuroscience research
- Accession number :
- edsair.doi.dedup.....63bb9e1d23c4f0d47467d9d56205d980