Evidence map›Paper›PMID 15847604›Full record

ArticleThe Biochemical journal2005

Ca2+ accumulation into acidic organelles mediated by Ca2+- and vacuolar H+-ATPases in human platelets.

José J López, Cristina Camello-Almaraz, José A Pariente, Ginés M Salido, Juan A Rosado

Open access · greenAbstract read
In one paragraph

Article in The Biochemical journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 127 citations in OpenAlex.

  1. Article
  2. Human platelets contain a pool of free zinc in dense granules.Research and practice in thrombosis and haemostasis · 2024
    Article
  3. Article
  4. Article
  5. Review
  6. GPN does not release lysosomal CaJournal of cell science · 2019
    Article
  7. Endolysosomal CaCancers · 2018
    Review
  8. Stanniocalcin 2 Regulates Non-capacitative CaFrontiers in physiology · 2018
    Article
  9. TRPs in Pain Sensation.Frontiers in physiology · 2017
    Review
  10. Article
  11. Two-Pore Channels and Parkinson's Disease: Where's the Link?Messenger (Los Angeles, Calif. : Print) · 2016
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Orais and STIMs: physiological mechanisms and disease.Journal of cellular and molecular medicine · 2012
    Review
  17. Article
  18. Article
  19. Article
  20. Review
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

5 authors at 1 institution in 1 country.

José J LópezDepartment of Physiology, University of Extremadura, 10071 Cáceres, Spain.
Cristina Camello-Almaraz
José A Pariente
Ginés M Salido
Juan A Rosado
Universidad de Extremadura · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most physiological agonists increase cytosolic free [Ca2+]c (cytosolic free Ca2+ concentration) to regulate a variety of cellular processes. How different stimuli evoke distinct spatiotemporal Ca2+ responses remains unclear, and the presence of separate intracellular Ca2+ stores might be of great functional relevance. Ca2+ accumulation into intracellular compartments mainly depends on the activity of Ca2+- and H+-ATPases. Platelets present two separate Ca2+ stores differentiated by the distinct sensitivity to thapsigargin and TBHQ [2,5-di-(t-butyl)-1,4-hydroquinone]. Although one store has long been identified as the dense tubular system, the nature of the TBHQ-sensitive store remains uncertain. Treatment of platelets with GPN (glycylphenylalanine-2-naphthylamide) impaired Ca2+ release by TBHQ and reduced that evoked by thrombin. In contrast, GPN did not modify Ca2+ mobilization stimulated by ADP or AVP ([arginine]vasopressin). Treatment with nigericin, a proton carrier, and bafilomycin A1, an inhibitor of the vacuolar H+-ATPase, to dissipate the proton gradient into acidic organelles induces a transient increase in [Ca2+]c that was abolished by previous treatment with the SERCA (sarcoplasmic/endoplasmic-reticulum Ca2+-ATPase) 3 inhibitor TBHQ. Depleted acidic stores after nigericin or bafilomycin A1 were refilled by SERCA 3. Thrombin, but not ADP or AVP, reduces the rise in [Ca2+]c evoked by nigericin and bafilomycin A1. Our results indicate that the TBHQ-sensitive store in human platelets is an acidic organelle whose Ca2+ accumulation is regulated by both Ca2+- and vacuolar H+-ATPases.

Indexed as

Adenosine DiphosphateArginine VasopressinBlood PlateletsCalciumCalcium-Transporting ATPasesCells, CulturedHumansHydrogen-Ion ConcentrationHydroquinonesMacrolidesOrganellesThrombinVacuolar Proton-Translocating ATPases2-tert-butylhydroquinoneAdenosine DiphosphateArginine Vasopressinbafilomycin A1CalciumCalcium-Transporting ATPasesHydroquinonesMacrolidesThrombinVacuolar Proton-Translocating ATPases

Identifiers

PMID15847604
PMCPMC1188269
OpenAlexW2111741341

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.