Evidence map›Paper›PMID 29564810›Full record

ArticleMolecular neurobiology2018

Kir6.2 Deficiency Promotes Mesencephalic Neural Precursor Cell Differentiation via Regulating miR-133b/GDNF in a Parkinson's Disease Mouse Model.

Yan Zhou, Jialei Zhu, Yang Lv, Chenghuan Song, Jianhua Ding, Ming Xiao, Ming Lu, Gang Hu

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed, 18 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Yan ZhouJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, China.
Jialei ZhuJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, China.
Yang LvJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, China.
Chenghuan SongJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, China.
Jianhua DingJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, China.
Ming XiaoJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, China.
Ming LuJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, China. lum@njmu.edu.cn.
Gang HuJiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, China. ghu@njmu.edu.cn.ORCID http://orcid.org/0000-0002-2864-4372
Nanjing Medical University · CNChina Pharmaceutical University · CNNanjing University of Chinese Medicine · CNShanghai Jiao Tong University · CN

Funding

National Natural Science Foundation of China 81473196National Natural Science Foundation of China 81573403National Natural Science Foundation of China 81603083National Natural Science Foundation of China 81630099National Natural Science Foundation of China 81773706Natural Science Foundation of the Higher Education Institutions of Jiangsu Province 15KJA310002
6 · The paper itself

Abstract

The loss of dopaminergic (DA) neurons in the substantia nigra (SN) is a major feature in the pathology of Parkinson's disease (PD). Using neural stem or progenitor cells (NSC/NPCs), the prospect of replacing the missing or damaged DA neurons is very attractive for PD therapy. However, little is known about the endogenous mechanisms and molecular pathways regulating the NSC/NPC proliferation and differentiation in the development of PD. Herein, using Kir6.2 knockout (Kir6.2

Indexed as

Cell Differentiation1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridinealpha-SynucleinAnimalsbeta CateninCell ProliferationDisease Models, AnimalDopaminergic NeuronsDown-RegulationGlial Cell Line-Derived Neurotrophic FactorGlycogen Synthase Kinase 3 betaHomeodomain ProteinsKcnj11 ChannelMesencephalonMice, Inbred C57BLMice, Knockout1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridinealpha-Synucleinbeta CateninGlial Cell Line-Derived Neurotrophic FactorGlycogen Synthase Kinase 3 betahomeobox protein PITX3Homeodomain ProteinsKcnj11 ChannelMicroRNAsMirn133 microRNA, mouseNr4a2 protein, mouseNuclear Receptor Subfamily 4, Group A, Member 2Potassium Channels, Inwardly RectifyingProbenecidProto-Oncogene Proteins c-bcl-2Transcription FactorsAdult neurogenesisDifferentiationKir6.2/K-ATPmiR-133bNurr1+ precursorsParkinson’s disease

Identifiers

PMID29564810
OpenAlexW2791562759

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.