Evidence map›Paper›PMID 35237256›Full record

ArticleFrontiers in immunology2022

PHLDA1 Suppresses TLR4-Triggered Proinflammatory Cytokine Production by Interaction With Tollip.

Hui Peng, Juping Wang, Xuhong Song, Jiangni Huang, Haoming Hua, Fanlu Wang, Ziyun Xu, Jing Ma, Jie Gao, Jing Zhao and 3 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

Hui PengDepartment of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High Cancer Incidence Coastal Chao Shan Area of Guang Dong Higher Education Institutes, Shantou University Medical College, Shantou, China.
Juping WangDepartment of Pathophysiology, School of Basic Medical Sciences, Youjiang Medical University for Nationalities, Baise, China.
Xuhong SongDepartment of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High Cancer Incidence Coastal Chao Shan Area of Guang Dong Higher Education Institutes, Shantou University Medical College, Shantou, China.
Jiangni HuangDepartment of Pathophysiology, School of Basic Medical Sciences, Youjiang Medical University for Nationalities, Baise, China.
Haoming HuaDepartment of Pathophysiology, School of Basic Medical Sciences, Youjiang Medical University for Nationalities, Baise, China.
Fanlu WangDepartment of Pathophysiology, School of Basic Medical Sciences, Youjiang Medical University for Nationalities, Baise, China.
Ziyun XuDepartment of Pathophysiology, School of Basic Medical Sciences, Youjiang Medical University for Nationalities, Baise, China.
Jing MaDepartment of Pathophysiology, School of Basic Medical Sciences, Youjiang Medical University for Nationalities, Baise, China.
Jie GaoDepartment of Pathophysiology, School of Basic Medical Sciences, Youjiang Medical University for Nationalities, Baise, China.
Jing ZhaoDepartment of Pathophysiology, School of Basic Medical Sciences, Youjiang Medical University for Nationalities, Baise, China.
Anna NongDepartment of Pathophysiology, School of Basic Medical Sciences, Youjiang Medical University for Nationalities, Baise, China.
Dongyang HuangDepartment of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High Cancer Incidence Coastal Chao Shan Area of Guang Dong Higher Education Institutes, Shantou University Medical College, Shantou, China.
Bin LiangDepartment of Cell Biology and Genetics, Key Laboratory of Molecular Biology in High Cancer Incidence Coastal Chao Shan Area of Guang Dong Higher Education Institutes, Shantou University Medical College, Shantou, China.
Affiliated Hospital of Youjiang Medical University for Nationalities · CNShantou University Medical College · CNShantou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pleckstrin homology-like domain, family A, member 1 (PHLDA1) has been reported to be expressed in many mammalian tissues and cells. However, the functions and exact mechanisms of PHLDA1 remain unclear. In this study, we found that PHLDA1 expression was significantly altered in macrophages after exposure to lipopolysaccharide (LPS)

Indexed as

EndotoxemiaLipopolysaccharidesAnimalsCytokinesIntracellular Signaling Peptides and ProteinsMammalsMiceMyeloid Differentiation Factor 88NF-kappa BToll-Like Receptor 4Transcription FactorsCytokinesIntracellular Signaling Peptides and ProteinsLipopolysaccharidesMyeloid Differentiation Factor 88NF-kappa BPhlda1 protein, mouseTlr4 protein, mouseTollip protein, mouseToll-Like Receptor 4Transcription FactorsPHLDA1proinflammatory cytokinesuppressTLR4Tollip

Identifiers

PMID35237256
PMCPMC8882599
OpenAlexW4212967984

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.