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Cited by 22Cell death mechanisms and regulationProtein Kinase Regulation and GTPase SignalingEndoplasmic Reticulum Stress and Disease

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ERK1/2 are involved in low potassium-induced apoptotic signaling downstream of ASK1-p38 MAPK pathway in cultured cerebellar granule neurons

Yamagishi, Satoru, Matsumoto, Tomoya, Numakawa, Tadahiro, Yokomaku, Daisaku, Adachi, Naoki, Hatanaka, Hiroshi, Yamada, Masashi, Shimoke, Koji, Ikeuchi, Toshihiko·2005·Brain Research
DOI 10.1016/j.brainres.2005.01.041
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Abstract

We have recently reported that the ASK1-p38 MAPK pathway has an important role in the low potassium (LK)-induced apoptosis of cultured cerebellar granule neurons. In the present study, we observed that ERK1/2 were significantly activated 6 h after a change of medium from HK (high potassium) to LK. In addition, U0126, a specific inhibitor of MEKs, remarkably prevented the apoptosis of cultured cerebellar granule neurons. Then, we examined the mechanism underlying the activation of ERK1/2 in the LK-induced apoptotic pathway. The addition of SB203580, an inhibitor of p38 MAPK, suppressed the increase in the phosphorylation of ERK1/2 after the change to LK medium. Furthermore, we found that the expression of a constitutively active mutant of ASK1, an upstream kinase of p38 MAPK, enhanced the phosphorylation of ERK1/2. These results suggest that ERK1/2 play a crucial role in LK-induced apoptosis of cultured cerebellar granule neurons and that the LK-stimulated activation of ERK1/2 is regulated by the ASK1-p38 MAPK pathway.

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  • Inhibition of JNK and ERK elicited partial protection against K5-induced apoptosis in control CGN, as shown by reduced caspase-3 activation.

    “Inhibition of JNK and ERK elicited partial protection against K5-induced apoptosis in control CGN as shown by reduced caspase-3 activation as evaluated by WB (Fig. 5a, b) [35,36].”

    From PCSK9 regulates neuronal apoptosis by adjusting ApoER2 levels and signaling (2012) · cites this paper as [35]

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Metadata

Authors
Yamagishi, S., Matsumoto, T., Numakawa, T., Yokomaku, D., Adachi, N., Hatanaka, H., Yamada, M., Shimoke, K., & Ikeuchi, T.
Affiliations
  • Max Planck Society (DE)
  • Institute for Protein Research, The University of Osaka (JP)
  • Kansai University (JP)
Corresponding author
Ikeuchi, Toshihiko
ORCID
Venue
Brain Research
Publisher
Elsevier BV
Published
2005-03
Volume
1038
Issue
2
Pages
223-230
ISSN
0006-8993 (ISSN-L)
DOI
10.1016/j.brainres.2005.01.041
OpenAlex
W1993245057
Cited by
22
References
0
Citations by year
2026: 1 · 2025: 2 · 2021: 1 · 2016: 2 · 2014: 2 · 2013: 1 · 2012: 2
FWCI
0.88
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Brain Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Ministry of Education, Culture, Sports, Science and Technology
  • Smoking Research Foundation
  • European Molecular Biology Organization
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
Keywords
ERK1/2, low potassium, neuronal apoptosis, ASK1, p38 MAPK, cerebellar granule cells, MEK inhibition, U0126, SB203580, ERK1/2 phosphorylation
MeSH terms
Adenoviridae, Animals, Butadienes, Cells, Cultured, Cerebellum, Enzyme Inhibitors, Female, Immunohistochemistry, Male, Neurons, Nitriles, Potassium Deficiency, Tetrazolium Salts, Thiazoles, Blotting, Western, Signal Transduction, Rats, Wistar, Apoptosis, Extracellular Signal-Regulated MAP Kinases, p38 Mitogen-Activated Protein Kinases, Mitogen-Activated Protein Kinase 7, MAP Kinase Kinase Kinase 5, Rats

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