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CORRECTION article

Front. Neurosci., 23 November 2023

Sec. Neurodegeneration

Volume 17 - 2023 | https://doi.org/10.3389/fnins.2023.1201109

Corrigendum: Proteomic profiling reveals the potential mechanisms and regulatory targets of sirtuin 4 in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's mouse model

  • 1. Department of Neurology, Fujian Medical University Union Hospital, Fuzhou, China

  • 2. Fujian Key Laboratory of Molecular Neurology, Institute of Neuroscience, Fujian Medical University, Fuzhou, China

  • 3. Cell Therapy Center, Xuanwu Hospital, Capital Medical University, Beijing, China

  • 4. The School of Basic Medical Sciences, Fujian Key Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Medical University, Fuzhou, China

  • 5. Department of Neurosurgery, General Hospital of Southern Theatre Command, PLA, Guangzhou, Guangdong, China

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In the published article, an error occurred in the representative immunoblot plot of TH in Figure 2B and Figure 8. The corrected Figure 2 and Figure 8 appear below.

Figure 2

Figure 2

SIRT4 plays a role in a PD model. (A) Flow chart of stereotactic injection of SIRT4-AAV virus and the establishment of a mouse model of PD induced by MPTP. (B) Representative western blots and densitometric analysis for TH protein between groups. TH protein extracts from substantia nigra after mice were intraperitoneally injected with saline and MPTP for 5 days. GAPDH was used as a loading control (n = 4 mice per group). (C) Representative western blots and densitometric analysis for SIRT4 protein between groups. SIRT4 protein extracts from substantia nigra after mice were intraperitoneally injected with saline or MPTP for 5 days. Tubulin was used as a loading control (n = 4 mice per group). (D, E) Representative western blots and densitometric analysis for DJ-1 or SIRT4 protein between groups, respectively. DJ-1 or SIRT4 protein extracts from substantia nigra of WT rats or DJ-1 KO rats. Tubulin was used as a loading control (n = 4 mice per group). All results are depicted as means ± SEM. The comparison across groups was analyzed by t-test. **P < 0.01, ***P < 0.001, and ****P < 0.0001 compared with the control group. TH, tyrosine hydroxylase; SIRT4, NAD-dependent protein lipoamidase sirtuin-4, mitochondrial.

Figure 8

Figure 8

Data visualizations of the results from the KEGG enrichment analysis of differentially expressed genes and proteins in SH-SY5Y cells after SIRT4 overexpression with ClueGO. A KEGG enrichment analysis of differentially expressed proteins in SH-SY5Y cells after SIRT4 overexpression was performed using ClueGO. The figure clearly shows the main proteins in the enriched pathways and the connection between A protein and different pathways. The size of the circle represents the number of different proteins.

The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.

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Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Summary

Keywords

Parkinson's disease, SIRT4, quantitative proteomic analysis, bioinformatics, biomarkers, FABP4, PPAR signaling pathway

Citation

Weng H, Song W, Fu K, Guan Y, Cai G, Huang E, Chen X, Zou H and Ye Q (2023) Corrigendum: Proteomic profiling reveals the potential mechanisms and regulatory targets of sirtuin 4 in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's mouse model. Front. Neurosci. 17:1201109. doi: 10.3389/fnins.2023.1201109

Received

06 April 2023

Accepted

08 November 2023

Published

23 November 2023

Volume

17 - 2023

Edited and reviewed by

Wen-Jun Tu, Chinese Academy of Medical Sciences and Peking Union Medical College, China

Updates

Copyright

*Correspondence: Qinyong Ye Haiqiang Zou

†These authors have contributed equally to this work and share first authorship

Disclaimer

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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