ArticleCellular and molecular neurobiology2013
CaMKII activates ASK1 to induce apoptosis of spinal astrocytes under oxygen-glucose deprivation.
Article in Cellular and molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 30 citations in OpenAlex.
- Review
- CaMKIIγ advances chronic intermittent hypoxia-induced cardiomyocyte apoptosis via HIF-1 signaling pathway.Sleep & breathing = Schlaf & Atmung · 2025Article
- TGFβ1-driven SMAD2/3 phosphorylation and myofibroblast emergence are fully dependent on the TGFβ1 pre-activation of MAPKs and controlled by maternal leucine zipper kinase.Cellular signalling · 2024Article
- Crystallographic mining of ASK1 regulators to unravel the intricate PPI interfaces for the discovery of small molecule.Computational and structural biotechnology journal · 2022Review
- Cardiac CaMKIIEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Calcium-induced dissociation of CIB1 from ASK1 regulates agonist-induced activation of the p38 MAPK pathway in platelets.The Biochemical journal · 2019Article
- Atorvastatin Attenuates Ischemia/Reperfusion-Induced Hippocampal Neurons Injury Via Akt-nNOS-JNK Signaling Pathway.Cellular and molecular neurobiology · 2017Article
- Impact of Heat Shock Protein A 12B Overexpression on Spinal Astrocyte Survival Against Oxygen-Glucose-Serum Deprivation/Restoration in Primary Cultured Astrocytes.Journal of molecular neuroscience : MN · 2016Article
- NQDI-1, an inhibitor of ASK1 attenuates acute perinatal hypoxic-ischemic cerebral injury by modulating cell death.Molecular medicine reports · 2016Article
- Cell Death Inducing Microbial Protein Phosphatase Inhibitors--Mechanisms of Action.Marine drugs · 2015Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium/calmodulin-dependent protein kinase II (CaMKII) is a ubiquitous, structurally complex multifunctional protein serine/threonine kinase that plays an important role in cell apoptosis via linking the ER stress and mitochondrial apoptosis pathways. Recently, CaMKII has been correlated with apoptosis signal-regulating kinase 1 (ASK1) activity and the ASK1-dependent apoptosis pathway through the direct phosphorylation of Thr845 of ASK1. The specific role of CaMKII in hypoxia-reoxygenation (H/R)-induced spinal astrocyte apoptosis, however, remains unclear. In this study, we investigated the effects of CaMKIIγ (an isoform of CaMKII) on spinal astrocyte apoptosis using an in vitro oxygen-glucose deprivation (OGD/R) model which mimics hypoxic/ischemic conditions in vivo. OGD/R increased cell death and the activation of CaMKII. Deletion of CaMKIIγ results in the reduced activation of CaMKII and apoptosis in astrocytes under OGD/R conditions. Notably, the deletion of CaMKIIγ induced ASK1 phosphorylation at Thr845 in astrocytes. The activation of JNK and p38 and the downstream effect of ASK1 were also reduced. These data suggest that CaMKIIγ is required for the CaMKII-dependent regulation of ASK1, affecting the apoptosis of a biologically important cell type under spinal cord injury.
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