ArticleProceedings of the National Academy of Sciences of the United States of America2021
Elongin functions as a loading factor for Mediator at ATF6α-regulated ER stress response genes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 citing papers in PubMed, 4 citations in OpenAlex.
- Elongin B orchestrates chromatin and transcriptional programs in H3K27M-mutant diffuse midline glioma.bioRxiv : the preprint server for biology · 2026Article
- The TFIIS N-terminal domain (TND): a transcription assembly module at the interface of order and disorder.Biochemical Society transactions · 2023Review
- Elongin functions as a loading factor for Mediator at ATF6α-regulated ER stress response genes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
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7 authors at 1 institution in 1 country.
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Abstract
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.
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