Evidence map›Paper›PMID 26245899›Full record

ArticleThe Journal of biological chemistry2015

Ca2+ Binding/Permeation via Calcium Channel, CaV1.1, Regulates the Intracellular Distribution of the Fatty Acid Transport Protein, CD36, and Fatty Acid Metabolism.

Dimitra K Georgiou, Adan Dagnino-Acosta, Chang Seok Lee, Deric M Griffin, Hui Wang, William R Lagor, Robia G Pautler, Robert T Dirksen, Susan L Hamilton

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Advances in CaChannels (Austin, Tex.) · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Equivalent L-type channel (CaBiochemical and biophysical research communications · 2020
    Article
  11. Review
  12. Article
  13. β-Subunit of the voltage-gated CaProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  14. A skeletal muscle L-type CaThe Journal of biological chemistry · 2018
    Article
  15. Article
  16. Review
  17. Article
  18. The CaNature communications · 2017
    Article
  19. BDA-410 Treatment Reduces Body Weight and Fat Content by Enhancing Lipolysis in Sedentary Senescent Mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2017
    Article
  20. Rimonabant improves metabolic parameters partially attributed to restoration of high voltage-activated Ca2+ channels in skeletal muscle in HFD-fed mice.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017
    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

9 authors at 2 institutions in 1 country.

Dimitra K GeorgiouFrom the Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030 and.
Adan Dagnino-AcostaFrom the Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030 and.
Chang Seok LeeFrom the Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030 and.
Deric M GriffinFrom the Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030 and.
Hui WangFrom the Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030 and.
William R LagorFrom the Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030 and.
Robia G PautlerFrom the Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030 and.
Robert T Dirksenthe Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, New York 14642.
Susan L HamiltonFrom the Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030 and susanh@bcm.edu.
Baylor College of Medicine · USUniversity of Rochester Medical Center · US

Funding

Basis of Muscle Dysfunction in Malignant Hyperthermia & Central Core DiseaseR01AR053349 · NIAMS · BAYLOR COLLEGE OF MEDICINE · PI DIRKSEN, ROBERT T, HAMILTON, SUSAN L · 2006 to 2020
$8.0M
Diabetes Endocrinology Research CenterP30DK079638 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI CHAN, LAWRENCE · 2008 to 2012
$6.4M
MODULATION OF SARCOPLASMIC RETICULUM CALCIUM RELEASER01AR041802 · NIAMS · BAYLOR COLLEGE OF MEDICINE · PI HAMILTON, SUSAN L, INGALLS, CHRISTOPHER · 1993 to 2014
$5.6M
NIAMS NIH HHS AR041802NIAMS NIH HHS AR053349NIAMS NIH HHS R01 AR041802NIAMS NIH HHS R01 AR053349NIDDK NIH HHS P30 DK079638
6 · The paper itself

Abstract

Ca(2+) permeation and/or binding to the skeletal muscle L-type Ca(2+) channel (CaV1.1) facilitates activation of Ca(2+)/calmodulin kinase type II (CaMKII) and Ca(2+) store refilling to reduce muscle fatigue and atrophy (Lee, C. S., Dagnino-Acosta, A., Yarotskyy, V., Hanna, A., Lyfenko, A., Knoblauch, M., Georgiou, D. K., Poché, R. A., Swank, M. W., Long, C., Ismailov, I. I., Lanner, J., Tran, T., Dong, K., Rodney, G. G., Dickinson, M. E., Beeton, C., Zhang, P., Dirksen, R. T., and Hamilton, S. L. (2015) Skelet. Muscle 5, 4). Mice with a mutation (E1014K) in the Cacna1s (α1 subunit of CaV1.1) gene that abolishes Ca(2+) binding within the CaV1.1 pore gain more body weight and fat on a chow diet than control mice, without changes in food intake or activity, suggesting that CaV1.1-mediated CaMKII activation impacts muscle energy expenditure. We delineate a pathway (Cav1.1→ CaMKII→ NOS) in normal skeletal muscle that regulates the intracellular distribution of the fatty acid transport protein, CD36, altering fatty acid metabolism. The consequences of blocking this pathway are decreased mitochondrial β-oxidation and decreased energy expenditure. This study delineates a previously uncharacterized CaV1.1-mediated pathway that regulates energy utilization in skeletal muscle.

Indexed as

AnimalsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Channels, L-TypeCD36 AntigensEnergy MetabolismFatty AcidsMaleMiceMice, TransgenicMitochondria, MuscleMuscle, SkeletalNitric Oxide SynthaseOxidation-ReductionCACNA1S protein, mouseCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Channels, L-TypeCD36 AntigensFatty AcidsNitric Oxide SynthaseCa2+/calmodulin-dependent protein kinase II (CaMKII)Ca2+ channelcalcium channelCaM kinase IICaV1.1CD36metabolic ratemetabolismmitochondriamitochondrial beta oxidationnitric-oxide synthaseskeletal muscleS-nitrosylation

Identifiers

PMID26245899
PMCPMC4583036
OpenAlexW2272626548

What OpenQuestion holds

Textmetadata
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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.