Evidence map›Paper›PMID 29615894›Full record

ArticleFrontiers in aging neuroscience2018

TRPC1 Deletion Causes Striatal Neuronal Cell Apoptosis and Proteomic Alterations in Mice.

Dian Wang, Haitao Yu, Benhong Xu, Hua Xu, Zaijun Zhang, Xiaohu Ren, Jianhui Yuan, Jianjun Liu, Yi Guo, Peter S Spencer and 1 more

Abstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
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  3. Review
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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

11 authors.

Dian WangCollege of Pharmacy, Jinan University, Guangzhou, China.
Haitao YuCollege of Pharmacy, Jinan University, Guangzhou, China.
Benhong XuKey Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
Hua XuCollege of Pharmacy, Jinan University, Guangzhou, China.
Zaijun ZhangInstitute of New Drug Research and Guangzhou, Key Laboratory of Innovative Chemical Drug Research in Cardio-Cerebrovascular Diseases, Jinan University College of Pharmacy, Guangzhou, China.
Xiaohu RenKey Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
Jianhui YuanKey Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
Jianjun LiuKey Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
Yi GuoDepartment of Neurology, Second Clinical College, Jinan University, Shenzhen, China.
Peter S SpencerDepartment of Neurology, School of Medicine, Oregon Institute of Occupational Health Sciences, Oregon Health and Science University, Portland, OR, United States.
Xifei YangKey Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transient receptor potential channel 1 (TRPC1) is widely expressed throughout the nervous system, while its biological role remains unclear. In this study, we showed that TRPC1 deletion caused striatal neuronal loss and significantly increased TUNEL-positive and 8-hydroxy-2'-deoxyguanosine (8-OHdG) staining in the striatum. Proteomic analysis by two-dimensional fluorescence difference gel electrophoresis (2D-DIGE) coupled with mass spectrometry (MS) revealed a total of 51 differentially expressed proteins (26 increased and 25 decreased) in the stratum of TRPC1 knockout (TRPC1

Indexed as

apoptosisER stress responseproteomicsstriatumTRPC1 deletion

Identifiers

PMID29615894
PMCPMC5870053

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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.