Evidence map›Paper›PMID 11713265›Full record

ArticleMolecular and cellular biology2001

Resistance to tumor necrosis factor-induced cell death mediated by PMCA4 deficiency.

K Ono, X Wang, J Han

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

29 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Plasma Membrane CaCancers · 2020
    Article
  5. ZnT2 is critical for lysosome acidification and biogenesis during mammary gland involution.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Plasma membrane calcium ATPases as novel candidates for therapeutic agent development.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2013
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. 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

3 authors at 1 institution in 1 country.

K OnoDepartment of Immunology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
X Wang
J Han
Scripps Research Institute · US

Funding

CELLULAR ACTIVATION MECHANISMS IN SEPTIC SHOCKR01AI041637 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI TOBIAS, PETER S · 1997 to 2012
$4.6M
NIAID NIH HHS AI 41637NIAID NIH HHS R01 AI041637
6 · The paper itself

Abstract

We used retrovirus insertion-mediated random mutagenesis to generate tumor necrosis factor (TNF)-resistant lines from L929 cells. Using this approach, we discovered that the plasma membrane calcium ATPase 4 (PMCA4) is required for TNF-induced cell death in L929 cells. Under basal conditions, PMCA4-deficient (PMCA(mut)) cells have a normal phenotype. However, stimulation with TNF induces an abnormal increase in the intracellular calcium concentration ([Ca(2+)](i)). The substantially elevated [Ca(2+)](i) caused resistance to TNF-induced cell death. We found that an increase in the total volume of acidic compartments (VAC), mainly constituted by lysosomes, is a common event in cell death caused by a variety of agonists. The increased [Ca(2+)](i) in PMCA(mut) cells promoted lysosome exocytosis, which, at least in part, accounted for the inhibition of TNF-induced increase in VAC and cell death. Promoting lysosome exocytosis by calcium inhibited TNF-induced cell death in wild-type L929 cells, while inhibition of lysosome exocytosis or increase of VAC by sucrose restored the sensitivity of PMCA(mut) cells to TNF-induced cell death. Thus, increase of the volume of acidic compartment is a part of the cell death process, and the antideath effect of calcium is mediated, at least in part, by inhibition of the TNF-induced increase in VAC.

Indexed as

Cell DeathAnimalsBase Sequencebeta-N-AcetylhexosaminidasesBlotting, WesternCalcimycinCalciumCalcium-Transporting ATPasesCation Transport ProteinsCell LineCell MembraneCell SurvivalCloning, MolecularDose-Response Relationship, DrugEndocytosisExocytosisbeta-N-AcetylhexosaminidasesCalcimycinCalciumCalcium-Transporting ATPasesCation Transport ProteinsLithium ChloridePlasma Membrane Calcium-Transporting ATPasesTumor Necrosis Factor-alpha

Identifiers

PMID11713265
PMCPMC99993
OpenAlexW2124817684

What OpenQuestion holds

Textmetadata
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.