Evidence map›Paper›PMID 27322654›Full record

ArticleNature immunology2016

The transcriptional repressor Hes1 attenuates inflammation by regulating transcription elongation.

Yingli Shang, Maddalena Coppo, Teng He, Fei Ning, Li Yu, Lan Kang, Bin Zhang, Chanyang Ju, Yu Qiao, Baohong Zhao and 3 more

Abstract read
In one paragraph

Article in Nature immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

61 citing papers in PubMed, 89 citations in OpenAlex.

  1. Ticagrelor IncreasesInternational journal of molecular sciences · 2020
    Trial
  2. Inferring Gene Regulatory Networks in Stem Cells: Methods and Applications.Methods in molecular biology (Clifton, N.J.) · 2027
    Review
  3. Article
  4. Neuroimmune Control of Inflammation in Acute Kidney Injury and Multiorgan Dysfunction.Journal of the American Society of Nephrology : JASN · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. ANKRD22 promotes resolution of psoriasiform skin inflammation by antagonizing NIK-mediated IL-23 production.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  16. Article
  17. Article
  18. Notch Signaling in Acute Inflammation and Sepsis.International journal of molecular sciences · 2023
    Review
  19. Involvement ofFrontiers in immunology · 2023
    Article
  20. Article

1 more citing papers are in PubMed but not listed here.

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

13 authors at 4 institutions in 3 countries.

Yingli ShangInstitute for Immunology and School of Medicine, Tsinghua University, Beijing. China.
Maddalena CoppoHospital for Special Surgery Research Division and the David Z. Rosensweig Genomics Center, New York, New York, USA.
Teng HeAcademy for Advanced Interdisciplinary Studies, Center for Quantitative Biology, and Peking-Tsinghua Center for Life Sciences, Peking University, Beijing, China.
Fei NingInstitute for Immunology and School of Medicine, Tsinghua University, Beijing. China.
Li YuInstitute for Immunology and School of Medicine, Tsinghua University, Beijing. China.
Lan KangInstitute for Immunology and School of Medicine, Tsinghua University, Beijing. China.
Bin ZhangInstitute for Immunology and School of Medicine, Tsinghua University, Beijing. China.
Chanyang JuHospital for Special Surgery Research Division and the David Z. Rosensweig Genomics Center, New York, New York, USA.ORCID 0000-0002-1213-1601
Yu QiaoHospital for Special Surgery Research Division and the David Z. Rosensweig Genomics Center, New York, New York, USA.
Baohong ZhaoHospital for Special Surgery Research Division and the David Z. Rosensweig Genomics Center, New York, New York, USA.
Manfred GesslerDevelopmental Biochemistry, Theodor-Boveri-Institute/Biocenter, and Comprehensive Cancer Center Mainfranken, Wuerzburg University, Wuerzburg, Germany.
Inez RogatskyHospital for Special Surgery Research Division and the David Z. Rosensweig Genomics Center, New York, New York, USA.
Xiaoyu HuInstitute for Immunology and School of Medicine, Tsinghua University, Beijing. China.ORCID 0000-0002-4289-6998
Tsinghua University · CNHospital for Special Surgery · USComprehensive Cancer Center Mainfranken · DEPeking University · CN

Funding

Glucocorticoid-regulated transcription networks in macrophage biologyR01DK099087 · NIDDK · HOSPITAL FOR SPECIAL SURGERY · PI INEZ ROGATSKY · 2014 to 2026
$6.0M
Regulation of Osteoclastogenesis and Arthritic Bone Resorption by RBP-JR01AR071463 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI Kyung-Hyun Park-Min · 2017 to 2026
$4.0M
Mechanisms of inflammatory bone remodelingR01AR068970 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI ZHAO, BAOHONG · 2016 to 2021
$1.9M
Regulation of Osteoclastogenesis and Arthritic Bone Resorption by RBP-JR00AR062047 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI ZHAO, BAOHONG · 2014 to 2016
$747k
NIAMS NIH HHS R00 AR062047NIAMS NIH HHS R01 AR068970NIAMS NIH HHS R01 AR071463NIDDK NIH HHS R01 DK099087
6 · The paper itself

Abstract

Most of the known regulatory mechanisms that curb inflammatory gene expression target pre-transcription-initiation steps, and evidence for post-initiation regulation of inflammatory gene expression remains scarce. We found that the transcriptional repressor Hes1 suppressed production of CXCL1, a chemokine that is crucial for recruiting neutrophils. Hes1 negatively regulated neutrophil recruitment in vivo in a manner that was dependent on macrophage-produced CXCL1, and it attenuated the severity of inflammatory arthritis. Mechanistically, inhibition of Cxcl1 expression by Hes1 did not involve modification of transcription initiation. Instead, Hes1 inhibited signal-induced recruitment of the positive transcription-elongation complex P-TEFb and thereby prevented phosphorylation of RNA polymerase II at Ser2 and productive elongation. Thus, our results identify Hes1 as a homeostatic suppressor of inflammatory responses that exerts its suppressive function by regulating transcription elongation.

Indexed as

AnimalsArthritisCell Cycle ProteinsCells, CulturedChemokine CXCL1Gene Expression RegulationInflammationMacrophagesMiceMice, Inbred C57BLMice, KnockoutMutationNeutrophil InfiltrationPositive Transcriptional Elongation Factor BRNA Polymerase IITranscription Elongation, GeneticCell Cycle ProteinsChemokine CXCL1Cxcl1 protein, mouseHes1 protein, mouseHey1 protein, mousePositive Transcriptional Elongation Factor BRNA Polymerase IITranscription Factor HES-1

Identifiers

PMID27322654
PMCPMC4955730
OpenAlexW2466341281

What OpenQuestion holds

Textmetadata
LicenceTDM
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.