Evidence map›Paper›PMID 25883416›Full record

ArticleMediators of inflammation2015

CNTNAP3 associated ATG16L1 expression and Crohn's disease.

Yu Qi Qiao, Mei Lan Huang, Qing Zheng, Tian Rong Wang, An Tao Xu, Yuan Cao, Di Zhao, Zhi Hua Ran, Jun Shen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Mediators of inflammation, 2015. 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
0.4field-weighted citation impact, top 37% 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, 6 citations in OpenAlex.

  1. Article
  2. Roles of Autophagy in Oxidative Stress.International journal of molecular sciences · 2020
    Review
  3. A Systematic Clinical Review of Prenatally Diagnosed Tetrasomy 9p.Balkan journal of medical genetics : BJMG · 2019
    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

9 authors at 1 institution in 1 country.

Yu Qi QiaoDivision of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China ; Shanghai Institute of Digestive Disease, Shanghai 200127, China ; Shanghai Inflammatory Bowel Disease Research Center, Shanghai 200127, China ; Key Laboratory of Gastroenterology & Hepatology, Ministry of Health (Shanghai Jiao Tong University), Shanghai 200127, China.ORCID 0000-0002-0374-5089
Mei Lan HuangDivision of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China ; Shanghai Institute of Digestive Disease, Shanghai 200127, China ; Shanghai Inflammatory Bowel Disease Research Center, Shanghai 200127, China ; Key Laboratory of Gastroenterology & Hepatology, Ministry of Health (Shanghai Jiao Tong University), Shanghai 200127, China.
Qing ZhengDivision of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China ; Shanghai Institute of Digestive Disease, Shanghai 200127, China ; Shanghai Inflammatory Bowel Disease Research Center, Shanghai 200127, China ; Key Laboratory of Gastroenterology & Hepatology, Ministry of Health (Shanghai Jiao Tong University), Shanghai 200127, China.
Tian Rong WangDivision of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China ; Shanghai Institute of Digestive Disease, Shanghai 200127, China ; Shanghai Inflammatory Bowel Disease Research Center, Shanghai 200127, China ; Key Laboratory of Gastroenterology & Hepatology, Ministry of Health (Shanghai Jiao Tong University), Shanghai 200127, China.
An Tao XuDivision of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China ; Shanghai Institute of Digestive Disease, Shanghai 200127, China ; Shanghai Inflammatory Bowel Disease Research Center, Shanghai 200127, China ; Key Laboratory of Gastroenterology & Hepatology, Ministry of Health (Shanghai Jiao Tong University), Shanghai 200127, China.
Yuan CaoDivision of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China ; Shanghai Institute of Digestive Disease, Shanghai 200127, China ; Shanghai Inflammatory Bowel Disease Research Center, Shanghai 200127, China ; Key Laboratory of Gastroenterology & Hepatology, Ministry of Health (Shanghai Jiao Tong University), Shanghai 200127, China.
Di ZhaoDivision of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China ; Shanghai Institute of Digestive Disease, Shanghai 200127, China ; Shanghai Inflammatory Bowel Disease Research Center, Shanghai 200127, China ; Key Laboratory of Gastroenterology & Hepatology, Ministry of Health (Shanghai Jiao Tong University), Shanghai 200127, China.
Zhi Hua RanDivision of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China ; Shanghai Institute of Digestive Disease, Shanghai 200127, China ; Shanghai Inflammatory Bowel Disease Research Center, Shanghai 200127, China ; Key Laboratory of Gastroenterology & Hepatology, Ministry of Health (Shanghai Jiao Tong University), Shanghai 200127, China.
Jun ShenDivision of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China ; Shanghai Institute of Digestive Disease, Shanghai 200127, China ; Shanghai Inflammatory Bowel Disease Research Center, Shanghai 200127, China ; Key Laboratory of Gastroenterology & Hepatology, Ministry of Health (Shanghai Jiao Tong University), Shanghai 200127, China.
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a common physiological process in cell homeostasis and regulation. Autophagy-related gene mutations and autophagy disorders are important in Crohn's disease (CD). The nucleotide oligomerization domain 2-autophagy genes autophagy 16-like 1 (NOD2-ATG16L1) signaling axis disorder contributes to the dysfunction of autophagy. This paper is focused on the relationship between contactin associated protein-like 3 (CNTNAP3) and ATG16L1 expression in Crohn's disease. The results indicated that the expression of ATG16L1 is higher in some CD patients compared to normal controls. ATG16L1 was well correlated with the C-reactive protein (CRP) in some CD patients. In vitro study revealed that CNTNAP3 could upregulate the expression of ATG16L1 and increase autophagy vacuoles.

Indexed as

Gene Expression RegulationAdultAutophagyAutophagy-Related ProteinsBiomarkersBiopsyCadaverineCarrier ProteinsCase-Control StudiesC-Reactive ProteinCrohn DiseaseFemaleHeLa CellsHumansMaleMembrane ProteinsATG16L1 protein, humanAutophagy-Related ProteinsBiomarkersCadaverineCarrier ProteinsCNTNAP3 protein, humanC-Reactive ProteinMembrane ProteinsmonodansylcadaverineNerve Tissue ProteinsRNA, Messenger

Identifiers

PMID25883416
PMCPMC4391322
OpenAlexW1994523053

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.