Evidence map›Paper›PMID 34673451›Full record

ArticleRedox biology2021

Kir6.2 is essential to maintain neurite features by modulating PM20D1-reduced mitochondrial ATP generation.

Nanshan Song, Yinquan Fang, Hong Zhu, Jiaqi Liu, Siyuan Jiang, Sifan Sun, Rong Xu, Jianhua Ding, Gang Hu, Ming Lu

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

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  8. Alzheimer's Disease-Associated SNP rs708727 inInternational journal of molecular sciences · 2022
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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

10 authors at 2 institutions in 1 country.

Nanshan SongJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, Nanjing, 211166, China.
Yinquan FangJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, Nanjing, 211166, China.
Hong ZhuJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, Nanjing, 211166, China.
Jiaqi LiuJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, Nanjing, 211166, China.
Siyuan JiangJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, Nanjing, 211166, China.
Sifan SunDepartment of Pharmacology, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Rong XuJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, Nanjing, 211166, China.
Jianhua DingJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, Nanjing, 211166, China.
Gang HuJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, Nanjing, 211166, China; Department of Pharmacology, Nanjing University of Chinese Medicine, Nanjing, 210023, China. Electronic address: ghu@njmu.edu.cn.
Ming LuJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, Nanjing, 211166, China; Neuroprotective Drug Discovery Key Laboratory, Department of Pharmacology, Nanjing Medical University, Nanjing, 211166, China. Electronic address: lum@njmu.edu.cn.
Nanjing Medical University · CNNanjing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kir6.2, a pore-forming subunit of the ATP-sensitive potassium (KATP) channels, regulates the functions of metabolically active tissues and acts as an ideal therapeutic target for multiple diseases. Previous studies have been conducted on peripheral kir6.2, but its precise physiological roles in the central nervous system (CNS) have rarely been revealed. In the current study, we evaluated the neurophenotypes and neuroethology of kir6.2 knockout (kir6.2

Indexed as

KATP ChannelsNeuritesAdenosine TriphosphateAmidohydrolasesAnimalsKcnj11 ChannelMiceMice, KnockoutMitochondriaPotassium Channels, Inwardly RectifyingAdenosine TriphosphateAmidohydrolasesKATP ChannelsKcnj11 ChannelPM20D1 protein, mousePotassium Channels, Inwardly RectifyingKATP channelsKir6.2Mitochondrial uncouplingNeuritePM20D1

Identifiers

PMID34673451
PMCPMC8577462
OpenAlexW3207250340

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.