Evidence map›Paper›PMID 20617337›Full record

ArticlePflugers Archiv : European journal of physiology2010

Inhibitors of Bcl-2 protein family deplete ER Ca2+ stores in pancreatic acinar cells.

Julia Gerasimenko, Pawel Ferdek, Lars Fischer, Anna S Gukovskaya, Stephen J Pandol

Open access · hybridAbstract read
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. On BH3 Mimetics and CaDrug development research · 2017
    Article
  7. BH3 mimetic-elicited CaCell death & disease · 2017
    Article
  8. Article
  9. Article
  10. Article
  11. The selective BH4-domain biology of Bcl-2-family members: IP3Rs and beyond.Cellular and molecular life sciences : CMLS · 2013
    Review
  12. Article
  13. 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

5 authors at 3 institutions in 2 countries.

Julia GerasimenkoThe Physiological Laboratory, University of Liverpool, Liverpool, L69 3BX, UK.
Pawel Ferdek
Lars Fischer
Anna S Gukovskaya
Stephen J Pandol
University of California System · USUniversity of Liverpool · GBUniversity of California, Los Angeles · US

Funding

The Southernearch Center for ALPD and CirrhosisP50AA011999 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HIDEKAZU TSUKAMOTO · 1999 to 2026
$45.8M
Medical Research Council G8801575NIAAA NIH HHS P50 AA011999NIAAA NIH HHS P60 AA11999Wellcome Trust
6 · The paper itself

Abstract

Physiological stimulation of pancreatic acinar cells by cholecystokinin and acetylcholine activate a spatial-temporal pattern of cytosolic [Ca(+2)] changes that are regulated by a coordinated response of inositol 1,4,5-trisphosphate receptors (IP(3)Rs), ryanodine receptors (RyRs) and calcium-induced calcium release (CICR). For the present study, we designed experiments to determine the potential role of Bcl-2 proteins in these patterns of cytosolic [Ca(+2)] responses. We used small molecule inhibitors that disrupt the interactions between prosurvival Bcl-2 proteins (i.e. Bcl-2 and Bcl-xl) and proapoptotic Bcl-2 proteins (i.e. Bax) and fluorescence microfluorimetry techniques to measure both cytosolic [Ca(+2)] and endoplasmic reticulum [Ca(+2)]. We found that the inhibitors of Bcl-2 protein interactions caused a slow and complete release of intracellular agonist-sensitive stores of calcium. The release was attenuated by inhibitors of IP(3)Rs and RyRs and substantially reduced by strong [Ca(2+)] buffering. Inhibition of IP(3)Rs and RyRs also dramatically reduced activation of apoptosis by BH3I-2'. CICR induced by different doses of BH3I-2' in Bcl-2 overexpressing cells was markedly decreased compared with control. The results suggest that Bcl-2 proteins regulate calcium release from the intracellular stores and suggest that the spatial-temporal patterns of agonist-stimulated cytosolic [Ca(+2)] changes are regulated by differential cellular distribution of interacting pairs of prosurvival and proapoptotic Bcl-2 proteins.

Indexed as

AnimalsApoptosisbcl-2-Associated X Proteinbcl-X ProteinBenzamidesBenzopyransCalciumCell Line, TumorEndoplasmic ReticulumInositol 1,4,5-Trisphosphate ReceptorsMaleMiceNitrilesPancreas, ExocrineProto-Oncogene Proteins c-bcl-2Rats3-iodo-5-chloro-N-(2-chloro-5-((4-chlorophenyl)sulphonyl)phenyl)-2-hydroxybenzamidebcl-2-Associated X ProteinBcl2l1 protein, mousebcl-X ProteinBenzamidesBenzopyransCalciumethyl 2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylateInositol 1,4,5-Trisphosphate ReceptorsNitrilesProto-Oncogene Proteins c-bcl-2Ryanodine Receptor Calcium Release Channel

Identifiers

PMID20617337
PMCPMC2937140
OpenAlexW2000601504

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.