Evidence map›Paper›PMID 23563987›Full record

ArticlePathology oncology research : POR2013

Prolyl isomerase Pin1 regulated signaling pathway revealed by Pin1 +/+ and Pin1 -/- mouse embryonic fibroblast cells.

Guo-Liang Huang, Jin-Hua Qiu, Bin-Bin Li, Jing-Jing Wu, Yan Lu, Xing-Yan Liu, Zhiwei He

Abstract read
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In one paragraph

Article in Pathology oncology research : POR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

1 citing paper in PubMed, 7 citations in OpenAlex.

  1. 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

7 authors at 3 institutions in 1 country.

Guo-Liang HuangSino-American Cancer Research Institute, Guangdong Medical College, No. 1 Xincheng Road, Dongguan, 523808, China.
Jin-Hua Qiu
Bin-Bin Li
Jing-Jing Wu
Yan Lu
Xing-Yan Liu
Zhiwei He
Key Laboratory of Guangdong Province · CNGuangdong Medical College · CNHuizhou Central People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pin1 (peptidylprolyl cis/trans isomerase, NIMA-interacting 1) plays a key role in a number of diseases including cancer and Alzheimer disease. Previous studies have identified a wide range of phosphoproteins as Pin1 substrates. Related pathways were analyzed separately. The aim of this study was to provide a comprehensive picture involving Pin1 regulation. A genome-wide mRNA expression microarray was carried out using the RNA isolation from Pin1 (+/+) and Pin1 (-/-) mouse embryonic fibroblast (MEF) cells. Signaling pathways regulated by Pin1 were analyzed with the utility of KEGG pathway and GO annotation. An expression pattern regulated by Pin1 was revealed. A total of 606 genes, 375 being up-regulated and 231 down-regulated, were differentially expressed when comparing Pin1 +/+ to Pin1 -/- MEF cells. Totally 48 pathways were shown to be regulated by Pin1 expression in KEGG pathway analysis. In the GO annotation system, 19 processes on biological processes, 15 processes on cellular components, and 18 processes on molecular functions were found to be in the regulation of Pin1 expression. Pathways related to immune system and cancer showed most significant association with Pin1 regulation. Pin1 is an important regulator in a wide range of signaling pathways that were related to immune system and cancer.

Indexed as

AnimalsCells, CulturedCluster AnalysisFibroblastsGene Expression ProfilingMiceMice, KnockoutNIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl IsomeraseReproducibility of ResultsSignal TransductionNIMA-Interacting Peptidylprolyl IsomerasePeptidylprolyl IsomerasePin1 protein, mouse

Identifiers

PMID23563987
OpenAlexW2083910368

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.