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Elongin functions as a loading factor for Mediator at ATF6α-regulated ER stress response genes

ABSTRACT: Elongin functions as a loading factor for Mediator at ATF6α-regulated ER stress response genes

PROVIDER: PRJNA722192 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14243400_1.fastq.gz	Fastqsanger.gz
	SRR14243400_2.fastq.gz	Fastqsanger.gz
	SRR14243401_1.fastq.gz	Fastqsanger.gz
	SRR14243401_2.fastq.gz	Fastqsanger.gz
	SRR14243402_1.fastq.gz	Fastqsanger.gz

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A role for Elongin in Mediator recruitment at ATF6α regulated genes [RNA-Seq]

Project description:The bZIP transcription factor ATF6α is a master regulator of endoplasmic reticulum (ER) stress response genes. In this report, we identify the multifunctional RNA polymerase II transcription factor Elongin as a cofactor for ATF6α-dependent transcription activation. Biochemical studies reveal that Elongin functions at least in part by facilitating ATF6α-dependent loading of Mediator at the promoters and enhancers of ER stress response genes. Depletion of Elongin from cells leads to impaired transcription of ER stress response genes and to defects in the recruitment of Mediator and, in particular, its CDK8 kinase subunit. Taken together, these findings bring to light a new role for Elongin as a loading factor for Mediator during the ER stress response.

2021-09-01 | GSE172125 | GEO

A role for Elongin in Mediator recruitment at ATF6α regulated genes [Cut&Tag]

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A role for Elongin in Mediator recruitment at ATF6α regulated genes [Cut&Tag]

Project description:A role for Elongin in Mediator recruitment at ATF6α regulated genes [Cut&Tag]

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A role for Elongin in Mediator recruitment at ATF6α regulated genes [RNA-Seq]

Project description:A role for Elongin in Mediator recruitment at ATF6α regulated genes [RNA-Seq]

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Elongin functions as a loading factor for Mediator at ATF6α-regulated ER stress response genes.

Project description:The bZIP transcription factor ATF6α is a master regulator of endoplasmic reticulum (ER) stress response genes. In this report, we identify the multifunctional RNA polymerase II transcription factor Elongin as a cofactor for ATF6α-dependent transcription activation. Biochemical studies reveal that Elongin functions at least in part by facilitating ATF6α-dependent loading of Mediator at the promoters and enhancers of ER stress response genes. Depletion of Elongin from cells leads to impaired transcription of ER stress response genes and to defects in the recruitment of Mediator and its CDK8 kinase subunit. Taken together, these findings bring to light a role for Elongin as a loading factor for Mediator during the ER stress response.

| S-EPMC8488631 | biostudies-literature

Elongin functions as a loading factor for Mediator at ATF6α-regulated ER stress response genes

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-08-30 | GSE172134 | GEO

Gene expression profiling of retinoic acid (RA)-treated embryoid bodies (EBs) derived from Elongin A+/+ and Elongin A-/- ES cells.

Project description:To identify potential Elongin A targets during neuronal differentiation of ES cells, a cDNA microarray analysis comparing embryoid bodies (EBs) derived from Elongin A+/+ ES cells and Elongin A-/- ES cells was performed. Gene expression in EBs derived from Elongin A+/+ and Elongin A-/- ES cells was measured at day 4 after retinoic acid treatment (2 ?M).

2011-07-25 | E-GEOD-30911 | biostudies-arrayexpress

Gene expression profiling of retinoic acid (RA)-treated embryoid bodies (EBs) derived from Elongin A+/+ and Elongin A-/- ES cells.

2011-07-26 | GSE30911 | GEO

Transcriptomic analysis of cellular senescence induced by ectopic expression of ATF6α in human breast cancer cells

Project description:To investigate the molecular mechanism that triggers endoplasmic reticulum (ER) stress-induced cellular senescence in breast cancer cells, we established MCF7 cell lines exposed to ATF6α ectopic expression. We then performed gene expression profiling analysis using data obtained from RNA-seq of 9 different cells at three time points.

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Development of miRNA expression signatures of MEFs deficient in a ER stress mediator XBP1 for tunicamycin treatment

Project description:To further development of our miRNA expression approach to ER stress, we have employed miRNA microarray expression profiling as a discovery platform to identify ER stress-responsible ones. Mouse embryonic fibroblasts (MEFs) deficient in a ER stress mediator XBP1 were treated with tunicamycin for 12 or 24 hrs. miRNAs responsible for tunicamycin-treatment for 12hrs in XBP1-dependent manner were extracted. Among them, expression of three miRNAs (miR-23a, miR-27a, miR-24-2) was quantified in the RNA samples from the same as the microarray, and COS7 cells by real-time PCR, confirming existence of similar mechanisms of trancriptional repression in ER stress by tunicamycin treatment. Mouse embryonic fibroblasts (MEFs) deficient in a ER stress mediator XBP1 were treated with 2ug/mL tunicamycin for 12 or 24 hrs. Two independent experiments were performed at each time (untreated, 12 or 24 hrs). miRNAs responsible for tunicamycin-treatment for 12hrs in XBP1-dependent manner were extracted.

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