Evidence map›Paper›PMID 32612143›Full record

ArticleScientific reports2020

Nurr1 performs its anti-inflammatory function by regulating RasGRP1 expression in neuro-inflammation.

Mihee Oh, Sun Young Kim, Jung-Eun Gil, Jeong-Su Byun, Dong-Wook Cha, Bonsu Ku, Woonghee Lee, Won-Kon Kim, Kyoung-Jin Oh, Eun-Woo Lee and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

27 citing papers in PubMed, 33 citations in OpenAlex.

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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

13 authors at 1 institution in 1 country.

Mihee OhBiodefense Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Republic of Korea.
Sun Young KimBiodefense Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Republic of Korea.
Jung-Eun GilBiodefense Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Republic of Korea.
Jeong-Su ByunBiodefense Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Republic of Korea.
Dong-Wook ChaBiodefense Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Republic of Korea.
Bonsu KuDisease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Republic of Korea.
Woonghee LeeMODNBIO Inc., Seoul, 08378, Republic of Korea.
Won-Kon KimMetabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Republic of Korea.
Kyoung-Jin OhMetabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Republic of Korea.
Eun-Woo LeeMetabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Republic of Korea.ORCID http://orcid.org/0000-0002-5156-0003
Kwang-Hee BaeMetabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Republic of Korea.
Sang Chul LeeMetabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Republic of Korea. lesach@kribb.re.kr.
Baek-Soo HanBiodefense Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Republic of Korea. bshan@kribb.re.kr.
Korea Research Institute of Bioscience and Biotechnology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nurr1, a transcription factor belonging to the orphan nuclear receptor, has an essential role in the generation and maintenance of dopaminergic neurons and is important in the pathogenesis of Parkinson' disease (PD). In addition, Nurr1 has a non-neuronal function, and it is especially well known that Nurr1 has an anti-inflammatory function in the Parkinson's disease model. However, the molecular mechanisms of Nurr1 have not been elucidated. In this study, we describe a novel mechanism of Nurr1 function. To provide new insights into the molecular mechanisms of Nurr1 in the inflammatory response, we performed Chromatin immunoprecipitation sequencing (ChIP-Seq) on LPS-induced inflammation in BV2 cells and finally identified the RasGRP1 gene as a novel target of Nurr1. Here, we show that Nurr1 directly binds to the RasGRP1 intron to regulate its expression. Moreover, we also identified that RasGRP1 regulates the Ras-Raf-MEK-ERK signaling cascade in LPS-induced inflammation signaling. Finally, we conclude that RasGRP1 is a novel regulator of Nurr1's mediated inflammation signaling.

Indexed as

AnimalsCell LineChromatinDNA-Binding ProteinsDopaminergic NeuronsGuanine Nucleotide Exchange FactorsHEK293 CellsHumansInflammationIntronsLipopolysaccharidesMiceMicrogliaNuclear Receptor Subfamily 4, Group A, Member 2Parkinson DiseaseSignal TransductionChromatinDNA-Binding ProteinsGuanine Nucleotide Exchange FactorsLipopolysaccharidesNR4A2 protein, humanNr4a2 protein, mouseNuclear Receptor Subfamily 4, Group A, Member 2RASGRP1 protein, humanRasgrp1 protein, mouseTranscription Factors

Identifiers

PMID32612143
PMCPMC7329810
OpenAlexW3039337921

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.