[Corrigendum] Neurotoxin β‑N‑methylamino‑L‑alanine induces endoplasmic reticulum stress‑mediated neuronal apoptosis

Shen,Haiying; Kim,Kiyoon; Oh,Yoojung; Yoon,Kyung Sik; Baik,Hyung Hwan; Kim,Sung Soo; Ha,Joohun; Kang,Insug; Choe,Wonchae

doi:10.3892/mmr.2018.9479

November-2018 Volume 18 Issue 5

Full Size Image

Journals

International Journal of Molecular Medicine

International Journal of Molecular Medicine is an international journal devoted to molecular mechanisms of human disease.

International Journal of Oncology

International Journal of Oncology is an international journal devoted to oncology research and cancer treatment.

Molecular Medicine Reports

Covers molecular medicine topics such as pharmacology, pathology, genetics, neuroscience, infectious diseases, molecular cardiology, and molecular surgery.

Oncology Reports

Oncology Reports is an international journal devoted to fundamental and applied research in Oncology.

Experimental and Therapeutic Medicine

Experimental and Therapeutic Medicine is an international journal devoted to laboratory and clinical medicine.

Oncology Letters

Oncology Letters is an international journal devoted to Experimental and Clinical Oncology.

Biomedical Reports

Explores a wide range of biological and medical fields, including pharmacology, genetics, microbiology, neuroscience, and molecular cardiology.

Molecular and Clinical Oncology

International journal addressing all aspects of oncology research, from tumorigenesis and oncogenes to chemotherapy and metastasis.

World Academy of Sciences Journal

Multidisciplinary open-access journal spanning biochemistry, genetics, neuroscience, environmental health, and synthetic biology.

International Journal of Functional Nutrition

Open-access journal combining biochemistry, pharmacology, immunology, and genetics to advance health through functional nutrition.

International Journal of Epigenetics

Publishes open-access research on using epigenetics to advance understanding and treatment of human disease.

Medicine International

An International Open Access Journal Devoted to General Medicine.

November-2018 Volume 18 Issue 5

Full Size Image

Correction Open Access

[Corrigendum] Neurotoxin β‑N‑methylamino‑L‑alanine induces endoplasmic reticulum stress‑mediated neuronal apoptosis

Authors:
- Haiying Shen
- Kiyoon Kim
- Yoojung Oh
- Kyung Sik Yoon
- Hyung Hwan Baik
- Sung Soo Kim
- Joohun Ha
- Insug Kang
- Wonchae Choe
View Affiliations / Copyright

Affiliations: Department of Biochemistry and Molecular Biology (BK21 Project), Medical Research Center for Bioreaction to Reactive Oxygen Species and Biomedical Science Institute, School of Medicine, Kyung Hee University, Seoul 130‑701, Republic of Korea

Copyright: © Shen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
Pages: 4768-4768
|
Published online on: September 12, 2018

https://doi.org/10.3892/mmr.2018.9479
Expand metrics +

Article

Mol Med Rep 14: [Related article:] 4873-4880, 2016; DOI: 10.3892/mmr.2016.5802

Following the publication of the above article and a Corrigendum published in July 2018, the authors have noted an additional error, associated with the presentation of Fig. 1C. Fig 1C showed that β-N-methylamino-L-alanine induces neuronal apoptotic cell death; however, an error was made in the compilation of this figure and an incorrect band image was selected for α-actinin, the loading control panel for Fig. 1C. A corrected version of Fig. 1 is shown opposite, incorporating the correct α-actinin protein bands in Fig. 1C. This change affects neither the interpretation of the data nor conclusions of this work.

Figure 1.

Effects of BMAA on cell viability and apoptosis of neuronal cells. (A) Neuronal cells were treated with 1.0, 2.0, or 3.0 mM BMAA and were analyzed at 24 h after the beginning of exposure to BMAA. The percentage cell viabilities are representative of at least three different experiments and are expressed as the mean ± standard deviation (*P<0.05 vs. untreated cells; #P<0.05 vs. 2.0 mM-treated cells). (B) The cell viabilities were measured at 12, 24 and 48 h after treatment with 2.0 mM BMAA. 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. 24 h-treated cells). (C) The cells were treated with increasing doses of BMAA (1.0, 2.0 and 3.0 mM) for 24 h. The protein expression levels of Bcl-2 family members, and the cleavage of caspase and PARP, were assessed by western blot analysis. α-actinin was used as a loading control. The data are representative of at least three different experiments. BMAA, β-N-methylamino-L-alanine; Bcl, B-cell lymphoma; Bax, Bcl-2-associated X protein; PARP, poly-ADP ribose polymerase.

We regret that this further error went unnoticed at the time, and thank the Editor for allowing us the opportunity to publish this additional Corrigendum.

Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

[Corrigendum] Neurotoxin β‑N‑methylamino‑L‑alanine induces endoplasmic reticulum stress‑mediated neuronal apoptosis

This article is mentioned in:

Article

Figure 1.

Related Articles