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关于MESH1基因敲低的转录反应和哺乳动物严谨反应的数据。

Data on the transcriptional response to MESH1 knockdown and mammalian stringent response.

作者信息

Sun Tianai, Ding Chien-Kuang Cornelia, Chi Jen-Tsan

机构信息

Department of Molecular Genetics and Microbiology, Duke University, Durham, NC 27710, United States.

Center for Genomic and Computational Biology, Duke University, Durham, NC 27708, United States.

出版信息

Data Brief. 2023 Jan 28;47:108938. doi: 10.1016/j.dib.2023.108938. eCollection 2023 Apr.

DOI:10.1016/j.dib.2023.108938
PMID:36761407
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9905932/
Abstract

MESH1 is the metazoan homolog of bacterial SpoT, the main phosphatase that dephosphorylates and degrades (p)ppGpp, the alarmone involved in the bacterial stringent response. The functional role of MESH1 in human cells is unknown. To define the global transcriptional response to MESH1 knockdown, we employed microarrays to perform transcriptome analysis of H1975 when the MESH1 was knocked down using three independent siRNAs targeting MESH1. The changes of each gene were derived by zero-transformation, followed by filtering to derive the genes affected by MESH1 knockdown. These datasets showed the transcriptional features of the mammalian stringent response and identified a prominent TAZ repression. Thus, we performed a second experiment to determine the contribution of TAZ repression to the transcriptional response of MESH1 knockdown by comparing the effects of MESH1-knockdown gene signatures in H1975 cells transduced with control or constitutive active TAZ (TAZS89A). The transcriptional response of these two cells to MESH1 was derived by zero transformation, followed by the effects of TAZ restoration to define the contribution of TAZ repression to the transcriptome features of human stringent response. The transcriptome data will be useful for the mechanistic understanding of the functional role of MESH1 in human cancer cells.

摘要

MESH1是细菌SpoT在后生动物中的同源物,SpoT是主要的磷酸酶,可使(p)ppGpp去磷酸化并降解,(p)ppGpp是参与细菌严谨反应的警报素。MESH1在人类细胞中的功能作用尚不清楚。为了确定对MESH1敲低的全局转录反应,我们使用微阵列对H1975进行转录组分析,此时使用三种独立的靶向MESH1的小干扰RNA(siRNA)敲低MESH1。每个基因的变化通过零转换得出,然后进行筛选以得出受MESH1敲低影响的基因。这些数据集显示了哺乳动物严谨反应的转录特征,并确定了显著的TAZ抑制。因此,我们进行了第二项实验,通过比较用对照或组成型活性TAZ(TAZS89A)转导的H1975细胞中MESH1敲低基因特征的影响,来确定TAZ抑制对MESH1敲低转录反应的贡献。这两种细胞对MESH1的转录反应通过零转换得出,随后通过TAZ恢复的影响来确定TAZ抑制对人类严谨反应转录组特征的贡献。转录组数据将有助于从机制上理解MESH1在人类癌细胞中的功能作用。

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本文引用的文献

1
Metazoan stringent-like response mediated by MESH1 phenotypic conservation via distinct mechanisms.后生动物中由MESH1介导的严格反应样反应通过不同机制实现表型保守。
Comput Struct Biotechnol J. 2022 May 6;20:2680-2684. doi: 10.1016/j.csbj.2022.05.001. eCollection 2022.
2
MESH1 knockdown triggers proliferation arrest through TAZ repression.MESH1 敲低通过抑制 TAZ 引发增殖停滞。
Cell Death Dis. 2022 Mar 10;13(3):221. doi: 10.1038/s41419-022-04663-6.
3
The regulation of ferroptosis by MESH1 through the activation of the integrative stress response.MESH1 通过激活整合应激反应来调节铁死亡。
Cell Death Dis. 2021 Jul 22;12(8):727. doi: 10.1038/s41419-021-04018-7.
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MESH1 is a cytosolic NADPH phosphatase that regulates ferroptosis.MESH1是一种调节铁死亡的胞质NADPH磷酸酶。
Nat Metab. 2020 Mar;2(3):270-277. doi: 10.1038/s42255-020-0181-1. Epub 2020 Mar 9.
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The Hippo Pathway Effector TAZ Regulates Ferroptosis in Renal Cell Carcinoma.Hippo 通路效应因子 TAZ 调控肾细胞癌中的铁死亡。
Cell Rep. 2019 Sep 3;28(10):2501-2508.e4. doi: 10.1016/j.celrep.2019.07.107.
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Kinome screen of ferroptosis reveals a novel role of ATM in regulating iron metabolism.铁死亡相关激酶组学筛选揭示 ATM 调控铁代谢的新功能
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