Evidence map›Paper›PMID 32439175›Full record

ArticleBiochemical and biophysical research communications2020

Pharmacological modulation and genetic deletion of REV-ERBα and REV-ERBβ regulates dendritic cell development.

Mohammed Amir, Sean Campbell, Theodore M Kamenecka, Laura A Solt

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

25 citing papers in PubMed, 32 citations in OpenAlex.

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  8. The Influence of Circadian Rhythms on DNA Damage Repair in Skin Photoaging.International journal of molecular sciences · 2024
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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

4 authors at 1 institution in 1 country.

Mohammed AmirDepartment of Immunology and Microbiology, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL, 33458, USA.
Sean CampbellDepartment of Immunology and Microbiology, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL, 33458, USA.
Theodore M KameneckaDepartment of Molecular Medicine, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL, 33458, USA.
Laura A SoltDepartment of Immunology and Microbiology, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL, 33458, USA; Department of Molecular Medicine, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL, 33458, USA. Electronic address: lsolt@scripps.edu.
Scripps Research Institute · US

Funding

Regulation of TH17 Cell Development and Function by the REV-ERBsR01AI116885 · NIAID · SCRIPPS FLORIDA · PI SOLT, LAURA A · 2016 to 2020
$2.1M
NIAID NIH HHS R01 AI116885
6 · The paper itself

Abstract

The nuclear receptors REV-ERBα and REV-ERBβ have been demonstrated to play key roles in the regulation of numerous physiological functions, such as metabolism and the circadian rhythm. Recent studies have established the REV-ERBs' roles in immunity, including macrophage and T cell responses. In contrast, their roles in dendritic cells have not been well defined. Dendritic cells are potent antigen presenting cells, connecting microbial sensing and innate immunity to adaptive immune responses. We demonstrate that both REV-ERBα and REV-ERBβ expression is upregulated during the course of bone marrow derived dendritic cell (BMDC) differentiation. BMDCs from REV-ERBα and REV-ERBβ deficient mice showed enhanced expression of maturation markers like CD86, MHCII, and proinflammatory cytokines. Conversely, treatment of BMDCs with a REV-ERB-specific agonist, SR9009, inhibited the expression of maturation markers and proinflammatory cytokines. Our study suggests the REV-ERBs act as negative regulators of dendritic cell development and activation. These results indicate that pharmacological modulation of REV-ERB activity could be an attractive strategy to modulate DC activation status and for DC-based therapies.

Indexed as

Gene DeletionGene Expression Regulation, DevelopmentalAnimalsBone Marrow CellsDendritic CellsFemaleMaleMice, Inbred C57BLNuclear Receptor Subfamily 1, Group D, Member 1PyrrolidinesReceptors, Cytoplasmic and NuclearRepressor ProteinsThiophenesNr1d1 protein, mouseNr1d2 protein, mouseNuclear Receptor Subfamily 1, Group D, Member 1PyrrolidinesReceptors, Cytoplasmic and NuclearRepressor ProteinsSR9009ThiophenesDendritic cellNR1D1NR1D2Nuclear receptorsREV-ERBSR9009

Identifiers

PMID32439175
PMCPMC7339779
OpenAlexW3027837791

What OpenQuestion holds

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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.