Evidence map›Paper›PMID 28293439›Full record

ArticleNeural plasticity2017

Proteomic Analysis of HDAC3 Selective Inhibitor in the Regulation of Inflammatory Response of Primary Microglia.

Mingxu Xia, Qiuchen Zhao, He Zhang, Yanting Chen, Zengqiang Yuan, Yun Xu, Meijuan Zhang

Open access · goldAbstract read
In one paragraph

Article in Neural plasticity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  8. HDAC3 Knockdown Dysregulates Juvenile Hormone and Apoptosis-Related Genes inInternational journal of molecular sciences · 2022
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  17. Inhibition of histone deacetylase 3 by MiR-494 alleviates neuronal loss and improves neurological recovery in experimental stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
    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

7 authors at 2 institutions in 1 country.

Mingxu XiaDepartment of Neurology, Affiliated Drum Tower Hospital, Nanjing University Medical school, Nanjing, Jiangsu 210008, China.ORCID 0000-0001-8460-4482
Qiuchen ZhaoDepartment of Neurology, Affiliated Drum Tower Hospital, Nanjing University Medical school, Nanjing, Jiangsu 210008, China.
He ZhangDepartment of Neurology, Affiliated Drum Tower Hospital, Nanjing University Medical school, Nanjing, Jiangsu 210008, China.
Yanting ChenDepartment of Neurology, Affiliated Drum Tower Hospital, Nanjing University Medical school, Nanjing, Jiangsu 210008, China.
Zengqiang YuanThe State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Yun XuDepartment of Neurology, Affiliated Drum Tower Hospital, Nanjing University Medical school, Nanjing, Jiangsu 210008, China.
Meijuan ZhangDepartment of Neurology, Affiliated Drum Tower Hospital, Nanjing University Medical school, Nanjing, Jiangsu 210008, China.ORCID 0000-0002-5375-5349
Nanjing Drum Tower Hospital · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HDAC3 has been shown to regulate inflammation. However, the role of HDAC3 in primary microglia is largely unknown. RGFP966 is a newly discovered selective HDAC3 inhibitor. In this study, we used protein mass spectrometry to analyze protein alterations in LPS-treated primary microglia with the application of RGFP966. Generally, about 2000 proteins were studied. 168 of 444 (37.8%) LPS-induced proteins were significantly reduced with the treatment of RGFP966, which mainly concentrated on Toll-like receptor signaling pathway. In this regard, we selected Toll-like receptor 2 (TLR2), TLR3, TLR6, MAPK p38, CD36, and spleen tyrosine kinase (SYK) for further validation and found that they were all significantly upregulated after LPS stimulation and downregulated in the presence of RGFP966. Additionally, RGFP966 inhibited supernatant tumor necrosis factor (TNF)-

Indexed as

AcrylamidesAnimalsCells, CulturedCerebral CortexEncephalitisHistone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesLipopolysaccharidesMiceMice, Inbred C57BLMicrogliaPhenylenediaminesProteomicsSTAT3 Transcription FactorSTAT5 Transcription FactorAcrylamidesHistone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesLipopolysaccharidesPhenylenediaminesRGFP966Stat3 protein, mouseSTAT3 Transcription FactorSTAT5 Transcription FactorToll-Like Receptor 2

Identifiers

PMID28293439
PMCPMC5331322
OpenAlexW2588859539

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.