Evidence map›Paper›PMID 19917257›Full record

ArticleMolecular cell2009

GM1-ganglioside accumulation at the mitochondria-associated ER membranes links ER stress to Ca(2+)-dependent mitochondrial apoptosis.

Renata Sano, Ida Annunziata, Annette Patterson, Simon Moshiach, Elida Gomero, Joseph Opferman, Michael Forte, Alessandra d'Azzo

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers.

0numbers the graph read from it
0cells of the map it votes in
164citing papers in PubMed
10.0field-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

164 citing papers in PubMed, 275 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Gangliosides in molecular interactions and cell regulation.The Journal of biological chemistry · 2026
    Review
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  6. Article
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  18. Cells · 2024
    Article
  19. Dysregulated inter-mitochondrial crosstalk in glioblastoma cells revealed by in situ cryo-electron tomography.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  20. Article

104 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

8 authors at 2 institutions in 1 country.

Renata SanoDepartment of Genetics and Tumor Cell Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Ida Annunziata
Annette Patterson
Simon Moshiach
Elida Gomero
Joseph Opferman
Michael Forte
Alessandra d'Azzo
St. Jude Children's Research Hospital · USOregon Health & Science University · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
GM1 as apoptotic signal in neurodegenerative GM1-gangliosidosisR01DK052025 · NIDDK · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI D'AZZO, ALESSANDRA · 1997 to 2010
$1.8M
GM1 at the ER-mitochondrion microdomains regulates Ca2+ signaling and apoptosisR01NS065951 · NINDS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI D'AZZO, ALESSANDRA · 2009 to 2010
$462k
GRADUATE RESEARCH SEMINAR IN BIOINORGANIC CHEMISTRYR13GM060905 · NIGMS · GORDON RESEARCH CONFERENCES · PI NUNEZ, MEGAN ELIZABETH · 2000 to 2000
$2k
FUNCTIONAL ROLES AND MECHANISMS OF SNO-RNAS IN PRE-RRNA PROCESSINGZ01DK052025 · NIDDK · DIABETES, DIGESTIVE, KIDNEY DISEASES · PI PECULIS, BRENDA A · 1996 to 2003
–
Intramural NIH HHS Z01 DK052025NCI NIH HHS CA021765NCI NIH HHS P30 CA021765NIDDK NIH HHS DK052025NIDDK NIH HHS R01 DK052025NIGMS NIH HHS GM060905NINDS NIH HHS R01 NS065951
6 · The paper itself

Abstract

Mitochondria-associated ER membranes, or MAMs, define the sites of endoplasmic reticulum/mitochondria juxtaposition that control Ca(2+) flux between these organelles. We found that in a mouse model of the human lysosomal storage disease GM1-gangliosidosis, GM1-ganglioside accumulates in the glycosphingolipid-enriched microdomain (GEM) fractions of MAMs, where it interacts with the phosphorylated form of IP3 receptor-1, influencing the activity of this channel. Ca(2+) depleted from the ER is then taken up by the mitochondria, leading to Ca(2+) overload in this organelle. The latter induces mitochondrial membrane permeabilization (MMP), opening of the permeability transition pore, and activation of the mitochondrial apoptotic pathway. This study identifies the GEMs as the sites of Ca(2+) diffusion between the ER and the mitochondria. We propose a new mechanism of Ca(2+)-mediated apoptotic signaling whereby GM1 accumulation at the GEMs alters Ca(2+) dynamics and acts as a molecular effector of both ER stress-induced and mitochondria-mediated apoptosis of neuronal cells.

Indexed as

ApoptosisAdenosine TriphosphateAnimalsbeta-GalactosidaseBrainCalciumCells, CulturedCytochromes cDisease Models, AnimalEndoplasmic ReticulumFibroblastsGangliosidosis, GM1GlycosphingolipidsG(M1) GangliosideHumansImmunoblottingAdenosine Triphosphatebeta-GalactosidaseCalciumCytochromes cGlycosphingolipidsG(M1) GangliosideInositol 1,4,5-Trisphosphate ReceptorsReactive Oxygen Species

Identifiers

PMID19917257
PMCPMC2782904
OpenAlexW2053599433

What OpenQuestion holds

Textmetadata
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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.