Evidence map›Paper›PMID 29679064›Full record

ArticleNature microbiology2018

Author Correction: Ephrin receptor A2 is an epithelial cell receptor for Epstein-Barr virus entry.

Hua Zhang, Yan Li, Hong-Bo Wang, Ao Zhang, Mei-Ling Chen, Zhi-Xin Fang, Xiao-Dong Dong, Shi-Bing Li, Yong Du, Dan Xiong and 11 more

Abstract readPublished Erratum
PubMed Publisher
In one paragraph

Article in Nature microbiology, 2018. 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
0.8field-weighted citation impact, top 35% 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, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 3 institutions in 2 countries.

Hua ZhangSun Yat-sen University Cancer Center; State Key Laboratory of Oncology, South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Yan LiDepartment of Pathology, Sun Yat-sen University Cancer Center, Guangzhou, China.
Hong-Bo WangGuangdong Provincial Key Laboratory of Liver Disease Research, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Ao ZhangSun Yat-sen University Cancer Center; State Key Laboratory of Oncology, South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Mei-Ling ChenSun Yat-sen University Cancer Center; State Key Laboratory of Oncology, South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Zhi-Xin FangSun Yat-sen University Cancer Center; State Key Laboratory of Oncology, South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Xiao-Dong DongSun Yat-sen University Cancer Center; State Key Laboratory of Oncology, South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Shi-Bing LiSun Yat-sen University Cancer Center; State Key Laboratory of Oncology, South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Yong DuSun Yat-sen University Cancer Center; State Key Laboratory of Oncology, South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Dan XiongSun Yat-sen University Cancer Center; State Key Laboratory of Oncology, South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Jiang-Yi HeSun Yat-sen University Cancer Center; State Key Laboratory of Oncology, South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Man-Zhi LiSun Yat-sen University Cancer Center; State Key Laboratory of Oncology, South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Yan-Min LiuSun Yat-sen University Cancer Center; State Key Laboratory of Oncology, South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Ai-Jun ZhouSun Yat-sen University Cancer Center; State Key Laboratory of Oncology, South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Qian ZhongSun Yat-sen University Cancer Center; State Key Laboratory of Oncology, South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Yi-Xin ZengSun Yat-sen University Cancer Center; State Key Laboratory of Oncology, South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Elliott KieffDepartment of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Zhiqiang ZhangImmunobiology and Transplant Science Center, Houston Methodist Research Institute, Houston, TX, USA.ORCID http://orcid.org/0000-0003-1796-081X
Benjamin E GewurzDepartment of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Bo ZhaoDepartment of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. bzhao@bwh.harvard.edu.ORCID http://orcid.org/0000-0002-8612-5597
Mu-Sheng ZengSun Yat-sen University Cancer Center; State Key Laboratory of Oncology, South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, China. zengmsh@sysucc.org.cn.ORCID http://orcid.org/0000-0003-3509-5591
Sun Yat-sen University · CNBrigham and Women's Hospital · USHouston Methodist · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the version of this Letter originally published, the authors reported on the use of 2,5-dimethylpyrrolyl benzoic acid to block Ephrin receptors. In 2011, it was reported that newly synthesized 2,5-dimethylpyrrolyl benzoic acid lacked the previously reported EphA2 antagonizing activity1. However, the purchased compound did in fact have the activity initially reported, suggesting that an uncharacterized alteration occurred during storage. The authors therefore wish to clarify that the compound used in their study should be more accurately referred to as a 2,5-dimethylpyrrolyl benzoic acid derivative. All references to 2,5-dimethylpyrrolyl benzoic acid in the Letter have now been changed to reflect this.Although 2,5-dimethylpyrrolyl benzoic acid derivatives have been reported to have off-target effects2, as do most small-molecule inhibitors, the multiple complementary methods and techniques used demonstrate that EphA2 is a key Epstein-Barr virus epithelial cell receptor. The conclusions of the study are therefore unchanged.

Identifiers

PMID29679064
OpenAlexW2802483635

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.