Evidence map›Paper›PMID 32152128›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

DBC1, p300, HDAC3, and Siah1 coordinately regulate ELL stability and function for expression of its target genes.

Subham Basu, Mahesh Barad, Dipika Yadav, Arijit Nandy, Bidisha Mukherjee, Jit Sarkar, Partha Chakrabarti, Satinath Mukhopadhyay, Debabrata Biswas

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Genetic variants inFrontiers in genetics · 2024
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  8. Article
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  11. Article
  12. Article
  13. Article
  14. RNAFrontiers in oncology · 2021
    Review
  15. 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

9 authors at 3 institutions in 1 country.

Subham BasuLaboratory of Transcription Biology, Molecular Genetics Division, Council of Scientific and Industrial Research (CSIR)-Indian Institute of Chemical Biology (IICB), Kolkata 700032, India.
Mahesh BaradLaboratory of Transcription Biology, Molecular Genetics Division, Council of Scientific and Industrial Research (CSIR)-Indian Institute of Chemical Biology (IICB), Kolkata 700032, India.
Dipika YadavLaboratory of Transcription Biology, Molecular Genetics Division, Council of Scientific and Industrial Research (CSIR)-Indian Institute of Chemical Biology (IICB), Kolkata 700032, India.
Arijit NandyLaboratory of Transcription Biology, Molecular Genetics Division, Council of Scientific and Industrial Research (CSIR)-Indian Institute of Chemical Biology (IICB), Kolkata 700032, India.
Bidisha MukherjeeDepartment of Endocrinology and Metabolism, Institute of Postgraduate Medical Education & Research (IPGM&R), Kolkata 700020, India.
Jit SarkarMetabolic Diseases Laboratory, Cell Biology and Physiology Division, CSIR-IICB, Kolkata 700032, India.
Partha ChakrabartiMetabolic Diseases Laboratory, Cell Biology and Physiology Division, CSIR-IICB, Kolkata 700032, India.
Satinath MukhopadhyayDepartment of Endocrinology and Metabolism, Institute of Postgraduate Medical Education & Research (IPGM&R), Kolkata 700020, India.
Debabrata BiswasLaboratory of Transcription Biology, Molecular Genetics Division, Council of Scientific and Industrial Research (CSIR)-Indian Institute of Chemical Biology (IICB), Kolkata 700032, India; dbiswas@iicb.res.in.
Indian Institute of Chemical Biology · INCouncil of Scientific and Industrial Research · INInstitute of Post Graduate Medical Education and Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Among all of the Super Elongation Complex (SEC) components, ELL1 (also known as ELL) is the only bona fide elongation factor that directly stimulates transcription elongation by RNA polymerase II. However, the mechanism(s) of functional regulation of ELL1 (referred to as ELL hereafter), through its stabilization, is completely unknown. Here, we report a function of human DBC1 in regulating ELL stability involving HDAC3, p300, and Siah1. Mechanistically, we show that p300-mediated site-specific acetylation increases, whereas HDAC3-mediated deacetylation decreases, ELL stability through polyubiquitylation by the E3 ubiquitin ligase Siah1. DBC1 competes with HDAC3 for the same binding sites on ELL and thus increases its acetylation and stability. Knockdown of DBC1 reduces ELL levels and expression of a significant number of genes, including those involved in glucose metabolism. Consistently, Type 2 diabetes patient-derived peripheral blood mononuclear cells show reduced expression of DBC1 and ELL and associated key target genes required for glucose homeostasis. Thus, we describe a pathway of regulating stability and functions of key elongation factor ELL for expression of diverse sets of genes, including ones that are linked to Type 2 diabetes pathogenesis.

Indexed as

Gene Expression RegulationAcetylationAdaptor Proteins, Signal TransducingAnimalsBinding SitesCell LineDiabetes Mellitus, Type 2E1A-Associated p300 ProteinGene Knockdown TechniquesGlucoseHistone Deacetylase 3Histone DeacetylasesHumansLeukocytes, MononuclearMutationNuclear ProteinsAdaptor Proteins, Signal TransducingCCAR2 protein, humanE1A-Associated p300 ProteinELL protein, humanEP300 protein, humanGlucoseHistone Deacetylase 3Histone DeacetylasesNuclear ProteinsSeven in Absentia ProteinsTranscriptional Elongation FactorsUbiquitin-Protein LigasesacetylationDBC1ELLtranscriptionubiquitylation

Identifiers

PMID32152128
PMCPMC7104407
OpenAlexW3009560374

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.