Evidence map›Paper›PMID 16549499›Full record

ArticleThe Journal of cell biology2006

Novel role of neuronal Ca2+ sensor-1 as a survival factor up-regulated in injured neurons.

Tomoe Y Nakamura, Andreas Jeromin, George Smith, Hideaki Kurushima, Hitoshi Koga, Yusaku Nakabeppu, Shigeo Wakabayashi, Junichi Nabekura

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
1.3field-weighted citation impact, top 24% 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

43 citing papers in PubMed, 65 citations in OpenAlex.

  1. Stress survival and longevity ofToxicology research · 2024
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  5. Distinct mechanism of TbPhysical chemistry chemical physics : PCCP · 2023
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  9. Use of Zebrafish Models to Boost Research in Rare Genetic Diseases.International journal of molecular sciences · 2021
    Review
  10. Calcium in Neuronal and Glial Response to Axotomy.International journal of molecular sciences · 2021
    Review
  11. Article
  12. Neuronal calcium sensor 1 (NCS1) dependent modulation of neuronal morphology and development.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  13. Article
  14. Calpain inhibitor and ibudilast rescue β cell functions in a cellular model of Wolfram syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Emerging Roles of Neuronal CaFrontiers in molecular neuroscience · 2019
    Review
  20. 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

8 authors at 5 institutions in 2 countries.

Tomoe Y NakamuraDepartment of Molecular Physiology, National Cardiovascular Center Research Institute, Suita, Osaka 565-8565, Japan. tomoen@ri.ncvc.go.jp
Andreas Jeromin
George Smith
Hideaki Kurushima
Hitoshi Koga
Yusaku Nakabeppu
Shigeo Wakabayashi
Junichi Nabekura
Kyushu University · JPNational Cerebral and Cardiovascular Center · JPBaylor College of Medicine · USJapan Science and Technology Agency · JPUniversity of Kentucky · US

Funding

GENE THERAPY FOR SPINAL CORD REGENERATIONR01NS038126 · NINDS · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI SMITH, GEORGE M · 1999 to 2006
$1.7M
NINDS NIH HHS NS38126NINDS NIH HHS R01 NS038126
6 · The paper itself

Abstract

A molecular basis of survival from neuronal injury is essential for the development of therapeutic strategy to remedy neurodegenerative disorders. In this study, we demonstrate that an EF-hand Ca2+-binding protein neuronal Ca2+ sensor-1 (NCS-1), one of the key proteins for various neuronal functions, also acts as an important survival factor. Overexpression of NCS-1 rendered cultured neurons more tolerant to cell death caused by several kinds of stressors, whereas the dominant-negative mutant (E120Q) accelerated it. In addition, NCS-1 proteins increased upon treatment with glial cell line-derived neurotrophic factor (GDNF) and mediated GDNF survival signal in an Akt (but not MAPK)-dependent manner. Furthermore, NCS-1 is significantly up-regulated in response to axotomy-induced injury in the dorsal motor nucleus of the vagus neurons of adult rats in vivo, and adenoviral overexpression of E120Q resulted in a significant loss of surviving neurons, suggesting that NCS-1 is involved in an antiapoptotic mechanism in adult motor neurons. We propose that NCS-1 is a novel survival-promoting factor up-regulated in injured neurons that mediates the GDNF survival signal via the phosphatidylinositol 3-kinase-Akt pathway.

Indexed as

AnimalsApoptosisAxotomyCalcium-Binding ProteinsCells, CulturedCell SurvivalChromonesEnzyme InhibitorsGene ExpressionGlial Cell Line-Derived Neurotrophic FactorGrowth SubstancesHydrogen PeroxideIn Situ Nick-End LabelingMorpholinesNeuronal Calcium-Sensor ProteinsNeurons2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneCalcium-Binding ProteinsChromonesEnzyme Inhibitorsfrequenin calcium sensor proteinsGlial Cell Line-Derived Neurotrophic FactorGrowth SubstancesHydrogen PeroxideMorpholinesNeuronal Calcium-Sensor ProteinsNeuropeptidesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-akt

Identifiers

PMID16549499
PMCPMC2063765
OpenAlexW2045634507

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.