Evidence map›Paper›PMID 26423071›Full record

ArticleImmunologic research2016

Low BIK outside-inside-out interactive inflammation immune-induced transcription-dependent apoptosis through FUT3-PMM2-SQSTM1-SFN-ZNF384.

Juxiang Huang, Lin Wang, Minghu Jiang, Qingchun Chen, Xiaoyu Zhang, Yangming Wang, Zhenfu Jiang, Zhongjie Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Immunologic research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.1field-weighted citation impact, top 45% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Overexpression and mutation ofTranslational cancer research · 2019
    Article
  3. Article
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

8 authors at 3 institutions in 1 country.

Juxiang HuangBiomedical Center, School of Electronic Engineering, Beijing University of Posts and Telecommunications, Beijing, 100876, China.
Lin WangBiomedical Center, School of Electronic Engineering, Beijing University of Posts and Telecommunications, Beijing, 100876, China. wanglin98@tsinghua.org.cn.
Minghu JiangLab of Computational Linguistics, School of Humanities and Social Sciences, Tsinghua University, Beijing, 100084, China.
Qingchun ChenBiomedical Center, School of Electronic Engineering, Beijing University of Posts and Telecommunications, Beijing, 100876, China.
Xiaoyu ZhangBiomedical Center, School of Electronic Engineering, Beijing University of Posts and Telecommunications, Beijing, 100876, China.
Yangming WangBiomedical Center, School of Electronic Engineering, Beijing University of Posts and Telecommunications, Beijing, 100876, China.
Zhenfu JiangBiomedical Center, School of Electronic Engineering, Beijing University of Posts and Telecommunications, Beijing, 100876, China.
Zhongjie ZhangCollege of Information, North China University of Technology, Beijing, 100043, China.
Beijing University of Posts and Telecommunications · CNNorth China University of Technology · CNTsinghua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Eighteen different Pearson mutual-positive-correlation BIK-activatory molecular feedback upstream and downstream networks were constructed from 79 overlapping of 376 GRNInfer and 98 Pearson under BIK CC ≥ 0.25 in low normal adjacent tissues of Taiwan compared with high lung adenocarcinoma. Our identified BIK interactive total feedback molecular network showed FUT3 [fucosyltransferase 3 (galactoside 3(4)-L-fucosyltransferase Lewis blood group)], PMM2 (phosphomannomutase 2), SQSTM1 (sequestosome 1), SFN_2 [REX2 RNA exonuclease 2 homolog (S. cerevisiae)] and ZNF384 (zinc finger protein 384) in low normal adjacent tissues of lung adenocarcinoma. BIK interactive total feedback terms included mitochondrial envelope, endomembrane system, integral to membrane, Golgi apparatus, cytoplasm, nucleus, cytosol, intracellular signaling cascade, mitochondrion, extracellular space, inflammation, immune response, apoptosis, cell differentiation, cell cycle, regulation of cell cycle, cell proliferation, estrogen-responsive protein Efp controls cell cycle and breast tumors growth, induction or regulation of apoptosis based on integrative GO, KEGG, GenMAPP, BioCarta and disease databases in low normal adjacent tissues of lung adenocarcinoma. Therefore, we propose low BIK outside-inside-out interactive inflammation immune-induced transcription-dependent apoptosis through FUT3-PMM2-SQSTM1-SFN-ZNF384 in normal adjacent tissues of lung adenocarcinoma.

Indexed as

Transcription, Genetic14-3-3 ProteinsAdenocarcinomaAdenocarcinoma of LungApoptosisApoptosis Regulatory ProteinsBiomarkers, TumorComputational BiologyExoribonucleasesGene Expression ProfilingGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansInflammationLung NeoplasmsMembrane Proteins14-3-3 ProteinsApoptosis Regulatory ProteinsBIK protein, humanBiomarkers, TumorExoribonucleasesMembrane ProteinsMitochondrial Proteinsphosphomannomutase 2, humanPhosphotransferases (Phosphomutases)Sequestosome-1 ProteinSFN protein, humanSQSTM1 protein, humanTrans-ActivatorsZNF384 protein, humanApoptosisBIK interactive networkInflammation immuneOutside-inside-outTranscription-dependent

Identifiers

PMID26423071
OpenAlexW2106259362

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.