Evidence map›Paper›PMID 28240257›Full record

ArticleScientific reports2017

Atlastin regulates store-operated calcium entry for nerve growth factor-induced neurite outgrowth.

Jing Li, Bing Yan, Hongjiang Si, Xu Peng, Shenyuan L Zhang, Junjie Hu

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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Neuronal Store-Operated Calcium Channels.Molecular neurobiology · 2023
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Endoplasmic Reticulum Lumenal Indicators inFrontiers in neuroscience · 2020
    Article
  12. Atlastin-mediated membrane tethering is critical for cargo mobility and exit from the endoplasmic reticulum.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  13. Neurite Collapse and Altered ER CaStem cell reports · 2019
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. 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 4 institutions in 2 countries.

Jing LiDepartment of Genetics and Cell Biology, College of Life Sciences, Nankai University, and Tianjin Key Laboratory of Protein Sciences, Tianjin 300071, China.
Bing YanNational Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Hongjiang SiDepartment of Medical Physiology, College of Medicine, Texas A&M Health Science Center, Temple, Texas, USA.
Xu PengDepartment of Medical Physiology, College of Medicine, Texas A&M Health Science Center, Temple, Texas, USA.
Shenyuan L ZhangDepartment of Medical Physiology, College of Medicine, Texas A&M Health Science Center, Temple, Texas, USA.
Junjie HuNational Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Texas A&M Health Science Center · USChinese Academy of Sciences · CNInstitute of Biophysics · CNNankai University · CN

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

Homotypic membrane fusion of the endoplasmic reticulum (ER) is mediated by a class of dynamin-like GTPases known as atlastin (ATL). Depletion of or mutations in ATL cause an unbranched ER morphology and hereditary spastic paraplegia (HSP), a neurodegenerative disease characterized by axon shortening in corticospinal motor neurons and progressive spasticity of the lower limbs. How ER shaping is linked to neuronal defects is poorly understood. Here, we show that dominant-negative mutants of ATL1 in PC-12 cells inhibit nerve growth factor (NGF)-induced neurite outgrowth. Overexpression of wild-type or mutant ATL1 or depletion of ATLs alters ER morphology and affects store-operated calcium entry (SOCE) by decreasing STIM1 puncta formation near the plasma membrane upon calcium depletion of the ER. In addition, blockage of the STIM1-Orai pathway effectively abolishes neurite outgrowth of PC-12 cells stimulated by NGF. These results suggest that SOCE plays an important role in neuronal regeneration, and mutations in ATL1 may cause HSP, partly by undermining SOCE.

Indexed as

Neuronal OutgrowthAnimalsCalciumCalcium SignalingCell LineEndoplasmic ReticulumExtracellular SpaceGene ExpressionGTP-Binding ProteinsHumansMembrane ProteinsNerve Growth FactorSpastic Paraplegia, HereditaryATL1 protein, humanCalciumGTP-Binding ProteinsMembrane ProteinsNerve Growth FactorNGF protein, human

Identifiers

PMID28240257
PMCPMC5327485
OpenAlexW2594397376

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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.