Evidence map›Paper›PMID 9147322›Full record

ArticleThe Journal of physiology1997

The immunophilin FK506-binding protein modulates Ca2+ release channel closure in rat heart.

R P Xiao, H H Valdivia, K Bogdanov, C Valdivia, E G Lakatta, H Cheng

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
11.3field-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

57 citing papers in PubMed, 180 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Calcium Signaling and Cardiac Arrhythmias.Circulation research · 2017
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
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  11. Effect of exercise training on Ca²⁺ release units of left ventricular myocytes of spontaneously hypertensive rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2014
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Elementary calcium release events from the sarcoplasmic reticulum in the heart.Advances in experimental medicine and biology · 2012
    Review
  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

6 authors at 2 institutions in 1 country.

R P XiaoLaboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
H H Valdivia
K Bogdanov
C Valdivia
E G Lakatta
H Cheng
National Institute on Aging · USNational Institutes of Health · US

Funding

Ryanodine Receptors, Calcium-dependent Arrhythmias & HCMR01HL055438 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI VALDIVIA, HECTOR H · 1996 to 2023
$8.0M
NHLBI NIH HHS HL55438
6 · The paper itself

Abstract

1. The nature of the signal that terminates the release of Ca2+ from the cardiac sarcoplasmic reticulum has remained elusive. This study was intended to examine whether FK506-binding protein (FKBP), which is tightly associated to the ryanodine receptor (RyR)/Ca2+ release channel, plays a role in the termination of Ca(2+)-induced Ca2+ release (CICR) in heart. 2. Confocal microscopy and the Ca2+ indicator fluo-3 were used to visualize the elementary release events, i.e. 'Ca2+ sparks' in rat ventricular myocytes under resting or voltage-clamped conditions. Additionally, electrophysiological single-channel recordings, at constant [Ca2+] or during [Ca2+] steps produced by photorelease of caged Ca2+, were obtained from rat cardiac RyRs incorporated in planar lipid bilayers. 3. Inhibition of FKBP by the immunosuppressants FK506 or rapamycin increased the duration of spontaneous or depolarization-evoked Ca2+ sparks 6- to 7-fold. In addition, Ca2+ sparks were seen with two-level amplitudes, corresponding to full and half normal spark amplitude. 4. FK506 potentiated and prolonged electrically stimulated [Ca2+]i transients and contractions, but did not affect the amplitude and kinetics of the L-type Ca2+ channel current. 5. In planar lipid bilayers, FK506 (15 microM) prolonged approximately 7-fold the mean open lifetime of reconstituted single RyRs, induced the appearance of long-lasting subconductance states, and markedly slowed the spontaneous decay of RyR activity elicited by fast and sustained Ca2+ stimuli. The time constant of the spontaneous decay of activity increased from 1.8 s in control to > or = 20 s in the presence of FK506. 6. We conclude that FKBP may afford an intrinsic mechanism to terminate RyR openings and it may thus exert a negative feedback on CICR in heart cells.

Indexed as

AnimalsCalciumCalcium ChannelsCalmodulin-Binding ProteinsCarrier ProteinsDNA-Binding ProteinsHeat-Shock ProteinsImmunosuppressive AgentsIon Channel GatingLipid BilayersMembrane PotentialsMuscle Fibers, SkeletalMuscle ProteinsMyocardiumPatch-Clamp TechniquesPolyenesCalciumCalcium ChannelsCalmodulin-Binding ProteinsCarrier ProteinsDNA-Binding ProteinsHeat-Shock ProteinsImmunosuppressive AgentsLipid BilayersMuscle ProteinsPolyenesRyanodine Receptor Calcium Release ChannelSirolimusTacrolimus Binding Proteins

Identifiers

PMID9147322
PMCPMC1159388
OpenAlexW2029974845

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.