Evidence map›Paper›PMID 28839191›Full record

ArticleScientific reports2017

Loss of Tmem30a leads to photoreceptor degeneration.

Lin Zhang, Yeming Yang, Shujin Li, Shanshan Zhang, Xiong Zhu, Zhengfu Tai, Mu Yang, Yuqing Liu, Xinzheng Guo, Bo Chen and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-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

16 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. The phosphatidylserine flippase β-subunit Tmem30a is essential for normal insulin maturation and secretion.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. The cell biology of the retinal pigment epithelium.Progress in retinal and eye research · 2020
    Review
  14. Animal models to study bile acid metabolism.Biochimica et biophysica acta. Molecular basis of disease · 2019
    Review
  15. Article
  16. 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

13 authors at 4 institutions in 2 countries.

Lin ZhangSichuan Provincial Key Laboratory for Human Disease Gene Study and School of Medicine, Hospital of the University of Electronic Science and Technology of China and Sichuan Provincial People's Hospital, Chengdu, Sichuan, 610072, China.
Yeming YangSichuan Provincial Key Laboratory for Human Disease Gene Study and School of Medicine, Hospital of the University of Electronic Science and Technology of China and Sichuan Provincial People's Hospital, Chengdu, Sichuan, 610072, China.
Shujin LiSichuan Provincial Key Laboratory for Human Disease Gene Study and School of Medicine, Hospital of the University of Electronic Science and Technology of China and Sichuan Provincial People's Hospital, Chengdu, Sichuan, 610072, China.
Shanshan ZhangSichuan Provincial Key Laboratory for Human Disease Gene Study and School of Medicine, Hospital of the University of Electronic Science and Technology of China and Sichuan Provincial People's Hospital, Chengdu, Sichuan, 610072, China.
Xiong ZhuSichuan Provincial Key Laboratory for Human Disease Gene Study and School of Medicine, Hospital of the University of Electronic Science and Technology of China and Sichuan Provincial People's Hospital, Chengdu, Sichuan, 610072, China.
Zhengfu TaiSichuan Provincial Key Laboratory for Human Disease Gene Study and School of Medicine, Hospital of the University of Electronic Science and Technology of China and Sichuan Provincial People's Hospital, Chengdu, Sichuan, 610072, China.
Mu YangSichuan Provincial Key Laboratory for Human Disease Gene Study and School of Medicine, Hospital of the University of Electronic Science and Technology of China and Sichuan Provincial People's Hospital, Chengdu, Sichuan, 610072, China.
Yuqing LiuSichuan Provincial Key Laboratory for Human Disease Gene Study and School of Medicine, Hospital of the University of Electronic Science and Technology of China and Sichuan Provincial People's Hospital, Chengdu, Sichuan, 610072, China.
Xinzheng GuoDepartment of Ophthalmology, Yale University School of Medicine, New Haven, CT, USA.
Bo ChenDepartment of Ophthalmology, Yale University School of Medicine, New Haven, CT, USA.
Zhilin JiangSichuan Provincial Key Laboratory for Human Disease Gene Study and School of Medicine, Hospital of the University of Electronic Science and Technology of China and Sichuan Provincial People's Hospital, Chengdu, Sichuan, 610072, China.
Fang LuSichuan Provincial Key Laboratory for Human Disease Gene Study and School of Medicine, Hospital of the University of Electronic Science and Technology of China and Sichuan Provincial People's Hospital, Chengdu, Sichuan, 610072, China. lufangfang@126.com.
Xianjun ZhuSichuan Provincial Key Laboratory for Human Disease Gene Study and School of Medicine, Hospital of the University of Electronic Science and Technology of China and Sichuan Provincial People's Hospital, Chengdu, Sichuan, 610072, China. xjzhu@uestc.edu.cn.
University of Electronic Science and Technology of China · CNSichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital · CNChengdu Institute of Biology · CNYale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phosphatidylserine (PS) is asymmetrically distributed between the outer and inner leaflets of the plasma membrane in eukaryotic cells. PS asymmetry on the plasma membrane depends on the activities of P4-ATPases, and disruption of PS distribution can lead to various disease conditions. Folding and transporting of P4-ATPases to their cellular destination requires the β subunit TMEM30A proteins. However, the in vivo functions of Tmem30a remain unknown. To this end, we generated retinal-specific Tmem30a-knockout mice to investigate its roles in vivo for the first time. Our data demonstrated that loss of Tmem30a in mouse cone cells leads to mislocalization of cone opsin, loss of photopic electroretinogram (ERG) responses and loss of cone cells. Mechanistically, Tmem30a-mutant mouse embryonic fibroblasts (MEFs) exhibited diminished PS flippase activity and increased exposure of PS on the cell surface. The broad loss of Tmem30a in adult mice led to a reduced scotopic photoresponse, mislocalization of ATP8A2 to the inner segment and cell body, and increased apoptosis in the retina. Our data demonstrated novel essential roles of Tmem30a in the retina.

Indexed as

Color VisionAdenosine TriphosphatasesAnimalsApoptosisCells, CulturedElectroretinographyMembrane ProteinsMice, KnockoutNight VisionOpsinsPhosphatidylserinesPhospholipid Transfer ProteinsProtein TransportRetinaRetinal Cone Photoreceptor CellsAdenosine TriphosphatasesATP8a2 protein, mouseMembrane ProteinsOpsinsPhosphatidylserinesPhospholipid Transfer ProteinsTMEM30a protein, mouse

Identifiers

PMID28839191
PMCPMC5571223
OpenAlexW2749652970

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.