Evidence map›Paper›PMID 28451724›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2017

Chronic loss of inhibitor-1 diminishes cardiac RyR2 phosphorylation despite exaggerated CaMKII activity.

Stefan Neef, Jordi Heijman, Kristian Otte, Matthias Dewenter, Ali R Saadatmand, Stefanie Meyer-Roxlau, Christopher L Antos, Johannes Backs, Dobromir Dobrev, Michael Wagner and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Stress-driven cardiac calcium mishandling via a kinase-to-kinase crosstalk.Pflugers Archiv : European journal of physiology · 2021
    Review
  5. Review
  6. Functions and therapeutic potential of protein phosphatase 1: Insights from mouse genetics.Biochimica et biophysica acta. Molecular cell research · 2019
    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

12 authors at 6 institutions in 2 countries.

Stefan NeefDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
Jordi HeijmanDepartment of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands.
Kristian OtteDepartment of Pharmacology and Toxicology, Carl Gustav Carus Faculty of Medicine, Technische Universität Dresden, Dresden, Germany.
Matthias DewenterDepartment of Pharmacology and Toxicology, Carl Gustav Carus Faculty of Medicine, Technische Universität Dresden, Dresden, Germany.
Ali R SaadatmandDepartment of Pharmacology and Toxicology, Carl Gustav Carus Faculty of Medicine, Technische Universität Dresden, Dresden, Germany.
Stefanie Meyer-RoxlauDepartment of Pharmacology and Toxicology, Carl Gustav Carus Faculty of Medicine, Technische Universität Dresden, Dresden, Germany.
Christopher L AntosDepartment of Pharmacology and Toxicology, Carl Gustav Carus Faculty of Medicine, Technische Universität Dresden, Dresden, Germany.
Johannes BacksDepartment of Cardiology, University of Heidelberg, Heidelberg, Germany.
Dobromir DobrevInstitute of Pharmacology, West German Heart and Vascular Center, University Duisburg-Essen, Essen, Germany.
Michael WagnerDepartment of Pharmacology and Toxicology, Carl Gustav Carus Faculty of Medicine, Technische Universität Dresden, Dresden, Germany.
Lars S MaierDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
Ali El-ArmoucheDepartment of Pharmacology and Toxicology, Carl Gustav Carus Faculty of Medicine, Technische Universität Dresden, Dresden, Germany. ali.el-armouche@tu-dresden.de.
TU Dresden · DEUniversity Hospital Carl Gustav Carus · DEUniversity Hospital Regensburg · DEHeidelberg University · DEMaastricht University · NLWest German Heart and Vascular Center Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inhibitor-1 (I-1) modulates protein phosphatase 1 (PP1) activity and thereby counteracts the phosphorylation by kinases. I-1 is downregulated and deactivated in failing hearts, but whether its role is beneficial or detrimental remains controversial, and opposing therapeutic strategies have been proposed. Overactivity of Ca

Indexed as

Adrenergic beta-1 Receptor AgonistsAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2DobutamineDogsEchocardiography, StressGuanine Nucleotide Exchange FactorsMice, KnockoutMyocardiumMyocytes, CardiacPhosphorylationProtein Phosphatase 1ProteinsRatsRyanodine Receptor Calcium Release ChannelStress, PhysiologicalAdrenergic beta-1 Receptor AgonistsCalcium-Calmodulin-Dependent Protein Kinase Type 2DobutamineEpac protein, mouseGuanine Nucleotide Exchange Factorsphosphoprotein phosphatase inhibitor 1Protein Phosphatase 1Proteinsryanodine receptor 2. mouseRyanodine Receptor Calcium Release ChannelCa2+/calmodulin-dependent protein kinase IIInhibitor-1Protein phosphatase 1Ryanodine receptor

Identifiers

PMID28451724
OpenAlexW2609090376

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.