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《适度流体剪切应力可通过激活FAK-MEK5-ERK5-cFos-AP1信号通路调节髓核细胞骨架及周围炎症介质》勘误

Corrigendum to "Moderate Fluid Shear Stress Could Regulate the Cytoskeleton of Nucleus Pulposus and Surrounding Inflammatory Mediators by Activating the FAK-MEK5-ERK5-cFos-AP1 Signaling Pathway".

作者信息

Ye Dongping, Liang Weiguo, Dai Libing, Yao Yicun

机构信息

Guangzhou City Red Cross Hospital, The Fourth Affiliated Hospital of Medical College, Jinan University, Guangzhou 510220, China.

出版信息

Dis Markers. 2018 Sep 27;2018:4597569. doi: 10.1155/2018/4597569. eCollection 2018.

DOI:10.1155/2018/4597569
PMID:30363744
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6180991/
Abstract

[This corrects the article DOI: 10.1155/2018/9405738.].

摘要

[本文更正了文章的数字对象标识符：10.1155/2018/9405738。]

相似文献

1
Corrigendum to "Moderate Fluid Shear Stress Could Regulate the Cytoskeleton of Nucleus Pulposus and Surrounding Inflammatory Mediators by Activating the FAK-MEK5-ERK5-cFos-AP1 Signaling Pathway".《适度流体剪切应力可通过激活FAK-MEK5-ERK5-cFos-AP1信号通路调节髓核细胞骨架及周围炎症介质》勘误
Dis Markers. 2018 Sep 27;2018:4597569. doi: 10.1155/2018/4597569. eCollection 2018.
2
Moderate Fluid Shear Stress Could Regulate the Cytoskeleton of Nucleus Pulposus and Surrounding Inflammatory Mediators by Activating the FAK-MEK5-ERK5-cFos-AP1 Signaling Pathway.适度的流体切应力可以通过激活 FAK-MEK5-ERK5-cFos-AP1 信号通路来调节核髓核和周围炎症介质的细胞骨架。
Dis Markers. 2018 Jun 12;2018:9405738. doi: 10.1155/2018/9405738. eCollection 2018.
3
MEK5 and ERK5 are localized in the nuclei of resting as well as stimulated cells, while MEKK2 translocates from the cytosol to the nucleus upon stimulation.MEK5和ERK5定位于静止及受刺激细胞的细胞核中，而MEKK2在受到刺激后从胞质溶胶转位至细胞核。
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Activation of either ERK1/2 or ERK5 MAP kinase pathways can lead to disruption of the actin cytoskeleton.细胞外信号调节激酶1/2（ERK1/2）或ERK5丝裂原活化蛋白激酶（MAPK）信号通路的激活均可导致肌动蛋白细胞骨架的破坏。
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本文引用的文献

1
Moderate Fluid Shear Stress Could Regulate the Cytoskeleton of Nucleus Pulposus and Surrounding Inflammatory Mediators by Activating the FAK-MEK5-ERK5-cFos-AP1 Signaling Pathway.适度的流体切应力可以通过激活 FAK-MEK5-ERK5-cFos-AP1 信号通路来调节核髓核和周围炎症介质的细胞骨架。
Dis Markers. 2018 Jun 12;2018:9405738. doi: 10.1155/2018/9405738. eCollection 2018.