Evidence map›Paper›PMID 31387986›Full record

ArticleExperimental & molecular medicine2019

The pore-forming subunit Kir6.1 of the K-ATP channel negatively regulates the NLRP3 inflammasome to control insulin resistance by interacting with NLRP3.

Ren-Hong Du, Ming Lu, Cong Wang, Jian-Hua Ding, Guangyu Wu, Gang Hu

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Do KFrontiers in immunology · 2024
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Kir6.1 and SUR2B in Cantú syndrome.American journal of physiology. Cell physiology · 2022
    Review
  8. Inward rectifier potassium (Kir) channels in the retina: living our vision.American journal of physiology. Cell physiology · 2022
    Review
  9. Review
  10. Article
  11. Article
  12. 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

6 authors at 3 institutions in 2 countries.

Ren-Hong DuJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, P. R. China.
Ming LuJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, P. R. China.
Cong WangJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, P. R. China.
Jian-Hua DingJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, P. R. China.
Guangyu WuDepartment of Pharmacology and Toxicology, Medical College of Georgia, Augusta University, 1459 Laney Walker Blvd., Augusta, 30912, Georgia, USA.
Gang HuJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, P. R. China. neuropha@njmu.edu.cn.
Nanjing Medical University · CNAugusta University · USNanjing University of Chinese Medicine · CN

Funding

Anterograde transport and signal regulation of GPCRsR01GM118915 · NIGMS · AUGUSTA UNIVERSITY · PI WU, GUANGYU · 2016 to 2019
$1.3M
National Natural Science Foundation of China (National Science Foundation of China) 81630099Natural Science Foundation of Jiangsu Province (Jiangsu Provincial Natural Science Foundation) BK20151559NIGMS NIH HHS R01 GM118915U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R01GM118915
6 · The paper itself

Abstract

Excessive activation of the NLRP3 inflammasome is a key component contributing to the pathogenesis of various inflammatory diseases. However, the molecular mechanisms underlying its activation and regulation remain poorly defined. The objective of this study was to explore the possible function of the K

Indexed as

Insulin ResistanceAnimalsCells, CulturedHEK293 CellsHumansInflammasomesIon Channel GatingKATP ChannelsMiceMice, Inbred C57BLMice, KnockoutMice, ObeseNLR Family, Pyrin Domain-Containing 3 ProteinProtein BindingProtein SubunitsInflammasomesKATP ChannelsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseProtein SubunitsuK-ATP-1 potassium channel

Identifiers

PMID31387986
PMCPMC6802643
OpenAlexW2965793313

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.