ArticleNeurochemical research2011
Negative feedback regulation of Raf/MEK/ERK cascade after sublethal cerebral ischemia in the rat hippocampus.
Article in Neurochemical research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Epidermal growth factor receptor modulation for neural repair: Implications for neurodegenerative disease therapy.Frontiers in molecular neuroscience · 2026Review
- Protective Effects of UCF-101 on Cerebral Ischemia-Reperfusion (CIR) is Depended on the MAPK/p38/ERK Signaling Pathway.Cellular and molecular neurobiology · 2016Article
- Rapamycin Reduced Ischemic Brain Damage in Diabetic Animals Is Associated with Suppressions of mTOR and ERK1/2 Signaling.International journal of biological sciences · 2016Article
- Profiling status epilepticus-induced changes in hippocampal RNA expression using high-throughput RNA sequencing.Scientific reports · 2014Article
- SUN11602, a novel aniline compound, mimics the neuroprotective mechanisms of basic fibroblast growth factor.ACS chemical neuroscience · 2013Article
- An L-type calcium channel agonist, bay K8644, extends the window of intervention against ischemic neuronal injury.Molecular neurobiology · 2013Article
- Intracellular signaling MAPK pathway after cerebral ischemia-reperfusion injury.Neurochemical research · 2012Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sublethal preconditioning ischemia protects neurons from lethal ischemia, and activation of ERK is associated with this protection. However, sublethal ischemia and reperfusion also results in rapid inactivation of ERK, which contributes to the dual-phase activation profile of ERK. In the present study, we observed sublethal ischemia-induced rapid inactivation of ERK was accompanied by phosphorylation of Raf-1 at Ser289/296/301 sites. Inhibition of calcium signaling by ketamine resulted in down-regulation of the Raf-1/ERK cascade and decreased phosphorylation of Raf-1 at Ser289/296/301. The MEK inhibitor U0126 suppressed ERK activity and phosphorylation of Raf-1 at Ser289/296/301 but not Raf-1 activation elicited by its dephosphorylation at S259 following ischemia. The PP2A inhibitor cantharidin but not Pin1 inhibitor juglone blocked Raf-1 dephosphorylation at Ser289/296/301 and ERK dephosphorylation and led to ERK sustained activation, which is associated with transcriptional up-regulation of genes related to differentiation. Furthermore, dual-phase activation of ERK did not alter the mRNA levels of genes related to proliferation or differentiation. These results indicate the initial robust activation of ERK phosphorylates Raf-1 at Ser289/296/301, resulting in Raf-1inhibition and then prompt inactivation of ERK following sublethal preconditioning ischemia. Dual-phase activation of ERK may exert its neuroprotection against lethal ischemia through blocking cell proliferation and differentiation.
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