Evidence map›Paper›PMID 16897576›Full record

ReviewJournal of muscle research and cell motility2006

New insights in the regulation of calcium transfers by muscle dystrophin-based cytoskeleton: implications in DMD.

Bruno Constantin, Stéphane Sebille, Christian Cognard

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Journal of muscle research and cell motility, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Myocardial late gadolinium enhancement is associated with clinical presentation in Duchenne muscular dystrophy carriers.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2016
    Article
  7. Article
  8. Article
  9. Effects of aging, exercise, and disease on force transfer in skeletal muscle.American journal of physiology. Endocrinology and metabolism · 2015
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Dystrobrevin controls neurotransmitter release and muscle Ca(2+) transients by localizing BK channels in Caenorhabditis elegans.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  15. Article
  16. Article
  17. Article
  18. Left ventricular T2 distribution in Duchenne muscular dystrophy.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2010
    Article
  19. Review
  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

3 authors at 2 institutions in 1 country.

Bruno ConstantinInstitut de Physiologie et Biologie Cellulaires, CNRS, UMR-6187, University of Poitiers, 86022, Poitiers, France. Bruno.Constantin@univ-poitiers.fr
Stéphane Sebille
Christian Cognard
Université de Poitiers · FRCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcium mishandling in Duchenne muscular dystrophy (DMD) suggested that dystrophin, a membrane-associated cytoskeleton protein, may regulate calcium-signalling cascades such as calcium entries. Calcium overload in human DMD myotubes is dependent on their contractile activity suggesting the involvement of channels being activated during contraction and/or calcium release. Forced expression of mini-dystrophin in dystrophin-deficient myotubes, reactivates appropriate sarcolemmal expression of dystrophin-associated proteins and restores normal calcium handling in the cytosol. Furthermore, the recombinant mini-dystrophin reduced the store-operated calcium influx across the sarcolemma, and the mitochondrial calcium uptake during this influx. A slow component of calcium release dependent on IP3R, as well as the production of IP3, were also reduced to normal levels by expression of mini-dystrophin. Our studies provide a new model for the convergent regulation of transmembrane calcium influx and IP3-dependent calcium release by the dystrophin-based cytoskeleton (DBC). We also suggest molecular association of such channels with DBC which may provide the scaffold for assembling a multiprotein-signalling complex that modulates the channel activity. This suggests that the loss of this molecular association could participate in the alteration of calcium homeostasis observed in DMD muscle cells.

Indexed as

AnimalsCalciumCalcium ChannelsCalcium SignalingCytoskeletonDystrophinHumansInositol 1,4,5-Trisphosphate ReceptorsMitochondriaMuscle Fibers, SkeletalMuscle, SkeletalMuscular Dystrophy, DuchenneCalciumCalcium ChannelsDystrophinInositol 1,4,5-Trisphosphate Receptors

Identifiers

PMID16897576
OpenAlexW2027619910

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.