Evidence map›Paper›PMID 32554466›Full record

ArticleThe Journal of biological chemistry2020

Phosphorylation of cardiac myosin-binding protein-C contributes to calcium homeostasis.

Mohit Kumar, Kobra Haghighi, Evangelia G Kranias, Sakthivel Sadayappan

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Early pathological mechanisms in a mouse model of heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  6. Cells · 2024
    Article
  7. Article
  8. Roles of cMyBP-C phosphorylation on cardiac contractile dysfunction inJournal of molecular and cellular cardiology plus · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Tetramisole is a new IPharmacology research & perspectives · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. Brugada Syndrome: Warning of a Systemic Condition?Frontiers in cardiovascular medicine · 2021
    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

4 authors at 1 institution in 1 country.

Mohit KumarHeart, Lung, and Vascular Institute, Division of Cardiovascular Health and Disease, Department of Internal Medicine, University of Cincinnati, Cincinnati, Ohio, USA.ORCID 0000-0002-3554-0563
Kobra HaghighiDepartment of Pharmacology and Systems Physiology, University of Cincinnati, Cincinnati, Ohio, USA.ORCID 0000-0002-3122-3894
Evangelia G KraniasDepartment of Pharmacology and Systems Physiology, University of Cincinnati, Cincinnati, Ohio, USA.ORCID 0000-0002-4621-6179
Sakthivel SadayappanHeart, Lung, and Vascular Institute, Division of Cardiovascular Health and Disease, Department of Internal Medicine, University of Cincinnati, Cincinnati, Ohio, USA sadayasl@ucmail.uc.edu.ORCID 0000-0003-2006-7678
University of Cincinnati · US

Funding

Fast myosin binding protein-C and cardiac contractility in heart failureR01HL105826 · NHLBI · UNIVERSITY OF CINCINNATI · PI SADAYAPPAN, SAKTHIVEL · 2011 to 2025
$4.5M
Skeletal Myosin-Binding Protein C (MyBP-C): Molecular Structure and FunctionR01AR067279 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CRAIG, ROGER W, WARSHAW, DAVID M · 2015 to 2019
$2.3M
IGF-2R is a new therapeutic target for cardiac ischemia-reperfusion injuryR01HL143490 · NHLBI · UNIVERSITY OF CINCINNATI · PI WANG, YIGANG · 2019 to 2022
$1.6M
Molecular mechanism of hypertrophic cardiomyopathy in populations of South Asian descendantsR01HL130356 · NHLBI · UNIVERSITY OF CINCINNATI · PI SADAYAPPAN, SAKTHIVEL · 2016 to 2019
$1.6M
Myoarchitectural Basis of Heart FailureR56HL139680 · NHLBI · OCEAN STATE RESEARCH INSTITUTE, INC. · PI GILBERT, RICHARD J · 2018 to 2018
$431k
NHLBI NIH HHS R01 HL105826NHLBI NIH HHS R01 HL130356NHLBI NIH HHS R01 HL143490NHLBI NIH HHS R56 HL139680NIAMS NIH HHS R01 AR067279
6 · The paper itself

Abstract

Cardiac myosin-binding protein-C (cMyBP-C) is highly phosphorylated under basal conditions. However, its phosphorylation level is decreased in individuals with heart failure. The necessity of cMyBP-C phosphorylation for proper contractile function is well-established, but the physiological and pathological consequences of decreased cMyBP-C phosphorylation in the heart are not clear. Herein, using intact adult cardiomyocytes from mouse models expressing phospho-ablated (AAA) and phosphomimetic (DDD) cMyBP-C as well as controls, we found that cMyBP-C dephosphorylation is sufficient to reduce contractile parameters and calcium kinetics associated with prolonged decay time of the calcium transient and increased diastolic calcium levels. Isoproterenol stimulation reversed the depressive contractile and Ca

Indexed as

HomeostasisAnimalsCalciumCarrier ProteinsMiceMyocardiumMyosin Binding Protein CPhosphorylationSarcomeresCalciumCarrier ProteinsMyosin Binding Protein Carrhythmiacalcium homeostasiscardiac arrhythmiacardiomyocytecardiomyopathycMyBP-Cheart failureHFpEFhypertrophic cardiomyopathyMYBPC3myofilamentomecamtiv mecarbilphosphorylationposttranslational modification calciumprotein phosphorylationsarcomere

Identifiers

PMID32554466
PMCPMC7415972
OpenAlexW3036863342

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.