Evidence map›Paper›PMID 32385332›Full record

ArticleNature communications2020

Negative elongation factor complex enables macrophage inflammatory responses by controlling anti-inflammatory gene expression.

Li Yu, Bin Zhang, Dinesh Deochand, Maria A Sacta, Maddalena Coppo, Yingli Shang, Ziyi Guo, Xiaomin Zeng, David A Rollins, Bowranigan Tharmalingam and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 42 citations in OpenAlex.

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  13. Review
  14. Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2023
    Article
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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

14 authors at 5 institutions in 2 countries.

Li Yu *Institute for Immunology and School of Medicine, Tsinghua University, Beijing, China.
Bin Zhang *Institute for Immunology and School of Medicine, Tsinghua University, Beijing, China.ORCID http://orcid.org/0000-0001-6232-6768
Dinesh DeochandHospital for Special Surgery Research Institute, The David Rosensweig Genomics Center, 535 East 70th Street, New York, NY, USA.ORCID http://orcid.org/0000-0002-7395-9250
Maria A SactaHospital for Special Surgery Research Institute, The David Rosensweig Genomics Center, 535 East 70th Street, New York, NY, USA.
Maddalena CoppoHospital for Special Surgery Research Institute, The David Rosensweig Genomics Center, 535 East 70th Street, New York, NY, USA.
Yingli ShangCollege of Veterinary Medicine, Shandong Agricultural University, Taian, China.
Ziyi GuoInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.
Xiaomin ZengInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.
David A RollinsHospital for Special Surgery Research Institute, The David Rosensweig Genomics Center, 535 East 70th Street, New York, NY, USA.
Bowranigan TharmalingamHospital for Special Surgery Research Institute, The David Rosensweig Genomics Center, 535 East 70th Street, New York, NY, USA.
Rong LiDepartment of Biochemistry & Molecular Medicine School of Medicine & Health Sciences, The George Washington University, 2300 I Street NW, Washington, DC, USA.
Yurii ChinenovHospital for Special Surgery Research Institute, The David Rosensweig Genomics Center, 535 East 70th Street, New York, NY, USA.
Inez RogatskyHospital for Special Surgery Research Institute, The David Rosensweig Genomics Center, 535 East 70th Street, New York, NY, USA. rogatskyi@hss.edu.ORCID http://orcid.org/0000-0003-3514-5077
Xiaoyu HuInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China. xiaoyuhu@tsinghua.edu.cn.ORCID http://orcid.org/0000-0002-4289-6998
Hospital for Special Surgery · USTsinghua University · CNKing Center · USGeorge Washington University · USShandong Agricultural University · CN

Funding

Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
Glucocorticoid-regulated transcription networks in macrophage biologyR01DK099087 · NIDDK · HOSPITAL FOR SPECIAL SURGERY · PI INEZ ROGATSKY · 2014 to 2026
$6.0M
Post-Initiation control of transcription in inflammatory macrophagesR01AI148129 · NIAID · HOSPITAL FOR SPECIAL SURGERY · PI ROGATSKY, INEZ · 2020 to 2024
$3.0M
Crosstalk between BRCA1 and Transcription in Breast CancerR01CA220578 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LI, RONG · 2017 to 2022
$2.1M
Regulation of Transcription Elongation in Adipose HomeostasisR01DK115219 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI DONG, LILY Q, LI, RONG · 2018 to 2021
$1.9M
ORTHOPAEDIC RESEARCH TRAININGT32AR007281 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI MAHER, SUZANNE A., VAN DER MEULEN, MARJOLEIN C · 1986 to 2018
$1.8M
NCI NIH HHS R01 CA220578NIAID NIH HHS R01 AI148129NIAMS NIH HHS T32 AR007281NIDDK NIH HHS R01 DK099087NIDDK NIH HHS R01 DK115219NIGMS NIH HHS T32 GM007739
6 · The paper itself

Abstract

Studies on macrophage gene expression have historically focused on events leading to RNA polymerase II recruitment and transcription initiation, whereas the contribution of post-initiation steps to macrophage activation remains poorly understood. Here, we report that widespread promoter-proximal RNA polymerase II pausing in resting macrophages is marked by co-localization of the negative elongation factor (NELF) complex and facilitated by PU.1. Upon inflammatory stimulation, over 60% of activated transcriptome is regulated by polymerase pause-release and a transient genome-wide NELF dissociation from chromatin, unexpectedly, independent of CDK9, a presumed NELF kinase. Genetic disruption of NELF in macrophages enhanced transcription of AP-1-encoding Fos and Jun and, consequently, AP-1 targets including Il10. Augmented expression of IL-10, a critical anti-inflammatory cytokine, in turn, attenuated production of pro-inflammatory mediators and, ultimately, macrophage-mediated inflammation in vivo. Together, these findings establish a previously unappreciated role of NELF in constraining transcription of inflammation inhibitors thereby enabling inflammatory macrophage activation.

Indexed as

Gene Expression RegulationAnimalsAnti-Inflammatory AgentsChromatinInflammationInterleukin-10Macrophage ActivationMacrophagesMiceNucleotide MotifsPromoter Regions, GeneticRNA Polymerase IITranscriptional ActivationTranscription FactorsTranscription, GeneticTranscription Initiation SiteAnti-Inflammatory AgentsChromatinInterleukin-10negative elongation factorRNA Polymerase IITranscription Factors

Identifiers

PMID32385332
PMCPMC7210294
OpenAlexW3020858642

What OpenQuestion holds

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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.