Evidence map›Paper›PMID 10811821›Full record

ArticleThe Journal of cell biology2000

Capacitative calcium entry deficits and elevated luminal calcium content in mutant presenilin-1 knockin mice.

M A Leissring, Y Akbari, C M Fanger, M D Cahalan, M P Mattson, F M LaFerla

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed
11.2field-weighted citation impact, top 1% 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

127 citing papers in PubMed, 331 citations in OpenAlex.

  1. Review
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  7. The Amyloid Precursor Protein Modulates the Position and Length of the Axon Initial Segment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
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  8. Article
  9. Review
  10. Dysregulated CaCells · 2022
    Review
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  17. APPsα rescues impaired CaProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  18. Review
  19. Review
  20. Article

67 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

M A LeissringLaboratory of Molecular Neuropathogenesis, Department of Neurobiology and Behavior, Center for the Neurobiology of Learning and Memory and Institute for Brain Aging and Dementia, University of California Irvine 92697-4561, USA.
Y Akbari
C M Fanger
M D Cahalan
M P Mattson
F M LaFerla
University of California, Irvine · USNational Institute on Aging · US

Funding

UC Irvine Alzheimer's Disease Research Center Induced Pluripotent Stem Cell CoreP50AG016573 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI LAFERLA, FRANK M · 2000 to 2019
$37.0M
Cellular And Molecular Pathogenesis Of Alzheimer'sZ01AG000312 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK P · 2001 to 2008
$1.9M
NIA NIH HHS AG16573NIA NIH HHS P50 AG016573
6 · The paper itself

Abstract

Dysregulation of calcium signaling has been causally implicated in brain aging and Alzheimer's disease. Mutations in the presenilin genes (PS1, PS2), the leading cause of autosomal dominant familial Alzheimer's disease (FAD), cause highly specific alterations in intracellular calcium signaling pathways that may contribute to the neurodegenerative and pathological lesions of the disease. To elucidate the cellular mechanisms underlying these disturbances, we studied calcium signaling in fibroblasts isolated from mutant PS1 knockin mice. Mutant PS1 knockin cells exhibited a marked potentiation in the amplitude of calcium transients evoked by agonist stimulation. These cells also showed significant impairments in capacitative calcium entry (CCE, also known as store-operated calcium entry), an important cellular signaling pathway wherein depletion of intracellular calcium stores triggers influx of extracellular calcium into the cytosol. Notably, deficits in CCE were evident after agonist stimulation, but not if intracellular calcium stores were completely depleted with thapsigargin. Treatment with ionomycin and thapsigargin revealed that calcium levels within the ER were significantly increased in mutant PS1 knockin cells. Collectively, our findings suggest that the overfilling of calcium stores represents the fundamental cellular defect underlying the alterations in calcium signaling conferred by presenilin mutations.

Indexed as

Calcium SignalingAlzheimer DiseaseAnimalsBombesinBradykininCalciumEndoplasmic ReticulumFibroblastsMembrane ProteinsMiceMice, Mutant StrainsPhosphatidylinositolsPresenilin-1BombesinBradykininCalciumMembrane ProteinsPhosphatidylinositolsPresenilin-1

Identifiers

PMID10811821
PMCPMC2174559
OpenAlexW2142474063

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.