Evidence map›Paper›PMID 25925952›Full record

ArticleThe Journal of biological chemistry2015

The Endoplasmic Reticulum Stress Sensor IRE1α in Intestinal Epithelial Cells Is Essential for Protecting against Colitis.

Hai-Sheng Zhang, Ying Chen, Li Fan, Qiu-Lei Xi, Guo-Hao Wu, Xiu-Xiu Li, Tang-Long Yuan, Sheng-Qi He, Yue Yu, Meng-Le Shao and 6 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

51 citing papers in PubMed, 69 citations in OpenAlex.

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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

16 authors at 5 institutions in 3 countries.

Hai-Sheng ZhangFrom the Laboratory of Food Safety Research, Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031.
Ying ChenFrom the Laboratory of Food Safety Research, Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031.
Li FanFrom the Laboratory of Food Safety Research, Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031.
Qiu-Lei Xithe Department of Surgery, Zhongshan Hospital, Fudan University School of Medicine, Shanghai 200030.
Guo-Hao Wuthe Department of Surgery, Zhongshan Hospital, Fudan University School of Medicine, Shanghai 200030.
Xiu-Xiu LiFrom the Laboratory of Food Safety Research, Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031.
Tang-Long YuanFrom the Laboratory of Food Safety Research, Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031.
Sheng-Qi HeFrom the Laboratory of Food Safety Research, Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031.
Yue YuFrom the Laboratory of Food Safety Research, Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031.
Meng-Le ShaoFrom the Laboratory of Food Safety Research, Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031.
Yang LiuFrom the Laboratory of Food Safety Research, Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031.
Chen-Guang Baithe Department of Pathology, Changhai Hospital, the Second Military Medical University, Shanghai 200433.
Zhi-Qiang Lingthe Department of Pathology, Zhejiang Cancer Research Institute, Zhejiang Cancer Hospital and Zhejiang Cancer Center, Hangzhou 310022.
Min Lithe Department of Surgery, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104.
Yong LiuFrom the Laboratory of Food Safety Research, Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, liuy@sibs.ac.cn.
Jing FangFrom the Laboratory of Food Safety Research, Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, the Department of Surgery, Zhongshan Hospital, Fudan University School of Medicine, Shanghai 200030, the Key Laboratory of Food Safety Risk Assessment, Ministry of Health, Beijing 100021, and jfang@sibs.ac.cn.
Chinese Academy of Sciences · CNSun Yat-sen University · CNSecond Military Medical University · CNShanghai Institute of Nutrition and Health · CNZhejiang Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intestinal epithelial cells (IECs) have critical roles in maintaining homeostasis of intestinal epithelium. Endoplasmic reticulum (ER) stress is implicated in intestinal epithelium homeostasis and inflammatory bowel disease; however, it remains elusive whether IRE1α, a major sensor of ER stress, is directly involved in these processes. We demonstrate here that genetic ablation of Ire1α in IECs leads to spontaneous colitis in mice. Deletion of IRE1α in IECs results in loss of goblet cells and failure of intestinal epithelial barrier function. IRE1α deficiency induces cell apoptosis through induction of CHOP, the pro-apoptotic protein, and sensitizes cells to lipopolysaccharide, an endotoxin from bacteria. IRE1α deficiency confers upon mice higher susceptibility to chemical-induced colitis. These results suggest that IRE1α functions to maintain the intestinal epithelial homeostasis and plays an important role in defending against inflammation bowel diseases.

Indexed as

AnimalsBase SequenceCell LineColitisDNA PrimersEndoplasmic ReticulumEndoribonucleasesHomeostasisIntestinal MucosaMiceMice, TransgenicPolymerase Chain ReactionProtein Serine-Threonine KinasesRNA, Small InterferingDNA PrimersEndoribonucleasesErn1 protein, mouseProtein Serine-Threonine KinasesRNA, Small Interferingcolitisendoplasmic reticulum stress (ER stress)inflammationinflammatory bowel disease (IBD)intestinal epithelium

Identifiers

PMID25925952
PMCPMC4463471
OpenAlexW2008572855

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.