Evidence map›Paper›PMID 31650360›Full record

ArticleNeurochemical research2019

PKC Mediates LPS-Induced IL-1β Expression and Participates in the Pro-inflammatory Effect of A

Sheng-Yu Fu, Ren-Ping Xiong, Yan Peng, Zhuo-Hang Zhang, Xing Chen, Yan Zhao, Ya-Lei Ning, Nan Yang, Yuan-Guo Zhou, Ping Li

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.4field-weighted citation impact, top 32% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
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  4. Review
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  6. Targeting the adenosine AChinese journal of traumatology = Zhonghua chuang shang za zhi · 2024
    Review
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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

10 authors at 1 institution in 1 country.

Sheng-Yu FuThe Molecular Biology Center, State Key Laboratory of Trauma, Burn and Combined Injury, Research Institute of Surgery and Daping Hospital, Third Military Medical University, Chongqing, 400042, China.
Ren-Ping XiongThe Molecular Biology Center, State Key Laboratory of Trauma, Burn and Combined Injury, Research Institute of Surgery and Daping Hospital, Third Military Medical University, Chongqing, 400042, China.
Yan PengThe Molecular Biology Center, State Key Laboratory of Trauma, Burn and Combined Injury, Research Institute of Surgery and Daping Hospital, Third Military Medical University, Chongqing, 400042, China.
Zhuo-Hang ZhangThe Molecular Biology Center, State Key Laboratory of Trauma, Burn and Combined Injury, Research Institute of Surgery and Daping Hospital, Third Military Medical University, Chongqing, 400042, China.
Xing ChenThe Molecular Biology Center, State Key Laboratory of Trauma, Burn and Combined Injury, Research Institute of Surgery and Daping Hospital, Third Military Medical University, Chongqing, 400042, China.
Yan ZhaoThe Molecular Biology Center, State Key Laboratory of Trauma, Burn and Combined Injury, Research Institute of Surgery and Daping Hospital, Third Military Medical University, Chongqing, 400042, China.
Ya-Lei NingThe Molecular Biology Center, State Key Laboratory of Trauma, Burn and Combined Injury, Research Institute of Surgery and Daping Hospital, Third Military Medical University, Chongqing, 400042, China.
Nan YangThe Molecular Biology Center, State Key Laboratory of Trauma, Burn and Combined Injury, Research Institute of Surgery and Daping Hospital, Third Military Medical University, Chongqing, 400042, China.
Yuan-Guo ZhouThe Molecular Biology Center, State Key Laboratory of Trauma, Burn and Combined Injury, Research Institute of Surgery and Daping Hospital, Third Military Medical University, Chongqing, 400042, China.
Ping LiThe Molecular Biology Center, State Key Laboratory of Trauma, Burn and Combined Injury, Research Institute of Surgery and Daping Hospital, Third Military Medical University, Chongqing, 400042, China. ping__ping0074@sina.com.ORCID http://orcid.org/0000-0002-4926-3835
Army Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathogens such as bacterial lipopolysaccharide (LPS) play an important role in promoting the production of the inflammatory cytokines interleukin-1 beta (IL-1β) and tumour necrosis factor-α (TNF-α) in response to infection or damage in microglia. However, whether different signalling pathways regulate these two inflammatory factors remains unclear. The protein kinase C (PKC) family is involved in the regulation of inflammation, and our previous research showed that the activation of the PKC pathway played a key role in the LPS-induced transformation of the adenosine A

Indexed as

AdenosineAdenosine A2 Receptor AgonistsAnimalsGlutamic AcidIndolesInflammationInterleukin-1betaLipopolysaccharidesMaleimidesMice, Inbred C57BLMicrogliaMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhenethylaminesProtein Kinase CProtein Kinase Inhibitors2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosineAdenosineAdenosine A2 Receptor AgonistsAdora2a protein, mousebisindolylmaleimide IGlutamic AcidIL1B protein, mouseIndolesInterleukin-1betaLipopolysaccharidesMaleimidesMapk1 protein, mouseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhenethylaminesProtein Kinase CProtein Kinase InhibitorsReceptor, Adenosine A2ARela protein, mouseTranscription Factor RelAIL-1β expressionInflammationLPSMicroglialProtein kinase CTNF-α expression

Identifiers

PMID31650360
OpenAlexW2981594646

What OpenQuestion holds

Textmetadata
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.