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修正:mRNA 输出调节因子 DBP5/DDX19、GLE1 或 IPPK(一种产生肌醇六磷酸的关键酶)的缺失,导致细胞质 mRNA 表达的差异改变和特定细胞缺陷。

Correction: Depletion of mRNA export regulator DBP5/DDX19, GLE1 or IPPK that is a key enzyme for the production of IP6, resulting in differentially altered cytoplasmic mRNA expression and specific cell defect.

作者信息

Okamura Masumi, Yamanaka Yasutaka, Shigemoto Maki, Kitadani Yuya, Kobayashi Yuhko, Kambe Taiho, Nagao Masaya, Kobayashi Issei, Okumura Katsuzumi, Masuda Seiji

出版信息

PLoS One. 2019 Jul 25;14(7):e0220511. doi: 10.1371/journal.pone.0220511. eCollection 2019.

DOI:10.1371/journal.pone.0220511
PMID:31344122
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6657908/
Abstract

[This corrects the article DOI: 10.1371/journal.pone.0197165.].

摘要

[本文更正了文章的数字对象标识符:10.1371/journal.pone.0197165。]

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5800/6657908/4a93051b4b4b/pone.0220511.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5800/6657908/4a93051b4b4b/pone.0220511.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5800/6657908/4a93051b4b4b/pone.0220511.g001.jpg

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Correction: Depletion of mRNA export regulator DBP5/DDX19, GLE1 or IPPK that is a key enzyme for the production of IP6, resulting in differentially altered cytoplasmic mRNA expression and specific cell defect.修正:mRNA 输出调节因子 DBP5/DDX19、GLE1 或 IPPK(一种产生肌醇六磷酸的关键酶)的缺失,导致细胞质 mRNA 表达的差异改变和特定细胞缺陷。
PLoS One. 2019 Jul 25;14(7):e0220511. doi: 10.1371/journal.pone.0220511. eCollection 2019.
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Depletion of mRNA export regulator DBP5/DDX19, GLE1 or IPPK that is a key enzyme for the production of IP6, resulting in differentially altered cytoplasmic mRNA expression and specific cell defect.mRNA 输出调节因子 DBP5/DDX19、GLE1 或 IPPK 的耗竭,这些因子是 IP6 产生的关键酶,导致细胞质 mRNA 表达的差异改变和特定的细胞缺陷。
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本文引用的文献

1
Depletion of mRNA export regulator DBP5/DDX19, GLE1 or IPPK that is a key enzyme for the production of IP6, resulting in differentially altered cytoplasmic mRNA expression and specific cell defect.mRNA 输出调节因子 DBP5/DDX19、GLE1 或 IPPK 的耗竭,这些因子是 IP6 产生的关键酶,导致细胞质 mRNA 表达的差异改变和特定的细胞缺陷。
PLoS One. 2018 May 10;13(5):e0197165. doi: 10.1371/journal.pone.0197165. eCollection 2018.