[Corrigendum] Neurotoxin β‑N‑methylamino‑L‑alanine induces endoplasmic reticulum stress‑mediated neuronal apoptosis
- Haiying Shen
- Kiyoon Kim
- Yoojung Oh
- Kyung Sik Yoon
- Hyung Hwan Baik
- Sung Soo Kim
- Joohun Ha
- Insug Kang
- Wonchae Choe
- Published online on: July 3, 2018 https://doi.org/10.3892/mmr.2018.9242
- Pages: 3115-3115
Copyright : © Shen et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY 4.0].
Mol Med Rep 14: [Related article:] 4873-4880, 2016; DOI: 10.3892/mmr.2016.5802
Following the publication of the article, the authors noted an error associated with the presentation of Fig. 4A. Fig 4 showed that overexpression of HSP70 suppresses ER stress-mediated neuronal death induced by β-N-methylamino-L-alanine (BMAA). An error was made in the compilation of this Figure, and the band images shown in the HA panel for Fig. 1A were selected incorrectly. A corrected version of Fig. 4 is shown below. This change affects neither the interpretation of the data nor conclusions of this work.
Overexpression of HSP70 suppresses ER stress-mediated neuronal death induced by BMAA, Tg and Tm. Following transfection with DNA constructs of pcDNA and HSP70 for 24 h, the cells were treated with 3.0 mM BMAA, 1 μM Tg, or 10 μg/ml Tm for 24 h. Con cells are untreated cells. (A) Western blotting for ER stress and apoptosis markers was performed. HSP70 was tagged with HA and the expression of HSP70 in the indicated transfectants was analyzed by western blotting. Consistent results are representative of at least three different experiments. (B) Cell viability was measured using an MTT assay. The percentage viability was plotted as the mean ± standard deviation of at least five experiments (*P<0.05 vs. untreated cells; #P<0.05 vs. BMAA-treated cells transfected with pcDNA only). (C) Nuclear morphology was visualized by DAPI nuclear staining. Mock are untransfected cells, and Con are untreated cells. The experiments were performed in triplicate, and cells were visualized under a confocal microscope. (D) The percentage of subG1 cells was analyzed via flow cytometry. The data are expressed as the mean ± standard deviation obtained from at least three independent experiments (*P<0.05 vs. untreated cells; #P<0.05 vs. BMAA-treated cells transfected with pcDNA only). BMAA, β-N-methylamino-L-alanine; Bcl, B-cell lymphoma; Bax, Bcl-2-associated X protein; P-, phosphorylated; ATF, transcription factor 6; ER, endoplasmic reticulum; CHOP, CCAAT/-enhancer-binding protein homologous protein; Tg, thapsigargin; Tm, tunicamycin; HSP, heat shock protein; HA, hemagglutinin; XBP, X-box binding protein; PARP, poly-ADP ribose polymerase; PDI, protein disulfide isomerase; PERK, protein kinase RNA-like endoplasmic reticulum kinase; con, control; eIF2, eukaryotic initiation factor 2.
We regret that this error occurred, and thank the Editor for allowing us the opportunity to publish this Corrigendum.