Evidence map›Paper›PMID 31611376›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

AFF1 acetylation by p300 temporally inhibits transcription during genotoxic stress response.

Nidhi Kumari, M Abul Hassan, Xiangdong Lu, Robert G Roeder, Debabrata Biswas

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 18 citations in OpenAlex.

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  10. Review
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  12. Differential microRNA Expression inJournal of clinical medicine · 2021
    Article
  13. DBC1, p300, HDAC3, and Siah1 coordinately regulate ELL stability and function for expression of its target genes.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  14. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Nidhi KumariLaboratory of Transcription Biology, Molecular Genetics Division, Council of Scientific and Industrial Research (CSIR)-Indian Institute of Chemical Biology (IICB), Kolkata 700032, India.
M Abul HassanLaboratory of Transcription Biology, Molecular Genetics Division, Council of Scientific and Industrial Research (CSIR)-Indian Institute of Chemical Biology (IICB), Kolkata 700032, India.
Xiangdong LuLaboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY 10065.
Robert G RoederLaboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY 10065 roeder@rockefeller.edu dbiswas@iicb.res.in.
Debabrata BiswasLaboratory of Transcription Biology, Molecular Genetics Division, Council of Scientific and Industrial Research (CSIR)-Indian Institute of Chemical Biology (IICB), Kolkata 700032, India; roeder@rockefeller.edu dbiswas@iicb.res.in.
Council of Scientific and Industrial Research · INRockefeller University · USIndian Institute of Chemical Biology · IN

Funding

Mechanisms of p53 target gene activation in DNA damage responsesR01CA129325 · NCI · ROCKEFELLER UNIVERSITY · PI ROEDER, ROBERT G · 2007 to 2011
$4.0M
Functional and Mechanistic Study of Histone Crotonylation in Hematological MalignanciesR01CA204639 · NCI · ROCKEFELLER UNIVERSITY · PI ALLIS, CHARLES DAVID, ARMSTRONG, SCOTT A · 2016 to 2020
$3.5M
DBT-Wellcome Trust India Alliance IA/I/14/1/501287NCI NIH HHS R01 CA129325NCI NIH HHS R01 CA204639Wellcome Trust
6 · The paper itself

Abstract

Soon after exposure to genotoxic reagents, mammalian cells inhibit transcription to prevent collisions with repair machinery and to mount a proper DNA damage response. However, mechanisms underlying early transcriptional inhibition are poorly understood. In this report, we show that site-specific acetylation of super elongation complex (SEC) subunit AFF1 by p300 reduces its interaction with other SEC components and impairs P-TEFb-mediated C-terminal domain phosphorylation of RNA polymerase II both in vitro and in vivo. Reexpression of wild-type AFF1, but not an acetylation mimic mutant, restores SEC component recruitment and target gene expression in AFF1 knockdown cells. Physiologically, we show that, upon genotoxic exposure, p300-mediated AFF1 acetylation is dynamic and strongly correlated with concomitant global down-regulation of transcription-and that this can be reversed by overexpression of an acetylation-defective AFF1 mutant. Therefore, we describe a mechanism of dynamic transcriptional regulation involving p300-mediated acetylation of a key elongation factor during genotoxic stress.

Indexed as

DNA DamageAcetylationDNA-Binding ProteinsDNA RepairE1A-Associated p300 ProteinGenomic InstabilityHumansPhosphorylationRNA Polymerase IIStress, PhysiologicalTranscriptional Elongation FactorsTranscription, GeneticAFF1 protein, humanDNA-Binding ProteinsE1A-Associated p300 ProteinEP300 protein, humanRNA Polymerase IITranscriptional Elongation FactorsacetylationDNA repairp300super elongation complextranscription

Identifiers

PMID31611376
PMCPMC6823056
OpenAlexW2980831600

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.