Evidence map›Paper›PMID 30598505›Full record

ArticleThe Journal of biological chemistry2019

Glutaredoxin 1 up-regulates deglutathionylation of α4 integrin and thereby restricts neutrophil mobilization from bone marrow.

Yuanyuan You, Junli Chen, Feimei Zhu, Qian Xu, Lu Han, Xiang Gao, Xiaoyu Zhang, Hongbo R Luo, Junming Miao, Xiaodong Sun and 8 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Dysregulation of the glutaredoxin/American journal of physiology. Cell physiology · 2020
    Article
  8. Article
  9. Review
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

18 authors at 4 institutions in 3 countries.

Yuanyuan YouFrom the Departments of Pathophysiology and.
Junli ChenFrom the Departments of Pathophysiology and.
Feimei ZhuFrom the Departments of Pathophysiology and.
Qian XuFrom the Departments of Pathophysiology and.
Lu Hanthe State Key Laboratory of Biotherapy and Cancer Center/Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu 610041, China.
Xiang Gaothe State Key Laboratory of Biotherapy and Cancer Center/Collaborative Innovation Center of Biotherapy, Sichuan University, Chengdu 610041, China.
Xiaoyu Zhangthe State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300020, China.
Hongbo R Luothe Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115.
Junming MiaoFrom the Departments of Pathophysiology and.
Xiaodong SunPharmacology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu 610041, China.
Hongyu RenFrom the Departments of Pathophysiology and.
Yu DuFrom the Departments of Pathophysiology and.
Lijuan GuoFrom the Departments of Pathophysiology and.
Xiaoying WangFrom the Departments of Pathophysiology and.
Yi WangFrom the Departments of Pathophysiology and.
Shanze ChenFrom the Departments of Pathophysiology and.
Ning HuangFrom the Departments of Pathophysiology and ninghuang2018@163.com.
Jingyu LiFrom the Departments of Pathophysiology and jingyuli@scu.edu.cn.ORCID 0000-0003-0997-9115
Sichuan University · CNBoston Children's Hospital · USChinese Academy of Medical Sciences & Peking Union Medical College · CNWest China Medical Center of Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

α4 integrin plays a crucial role in retention and release of neutrophils from bone marrow. Although α4 integrin is known to be a potential target of reactive oxygen species (ROS)-induced cysteine glutathionylation, the physiological significance and underlying regulatory mechanism of this event remain elusive. Here, using

Indexed as

Up-RegulationAnimalsBone MarrowDisease Models, AnimalGlutaredoxinsHL-60 CellsHumansInflammationIntegrin alpha4Mice, KnockoutNeutrophilsVascular Cell Adhesion Molecule-1Glrx protein, mouseGlutaredoxinsIntegrin alpha4Vascular Cell Adhesion Molecule-1glutaredoxinglutathionylationimmune responseinflammationintegrinneutrophilneutrophil mobilizationreactive oxygen species (ROS)vascular cell adhesion molecular 1 (VCAM-1)α4 integrin

Identifiers

PMID30598505
PMCPMC6393595
OpenAlexW2906918902

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.