Evidence map›Paper›PMID 31299211›Full record

ReviewCellular signalling2019

mAKAPβ signalosomes - A nodal regulator of gene transcription associated with pathological cardiac remodeling.

Kimberly Dodge-Kafka, Moriah Gildart, Kristin Tokarski, Michael S Kapiloff

Open access · greenAbstract readReview
In one paragraph

Review in Cellular signalling, 2019. 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
1.3field-weighted citation impact, top 20% 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, 26 citations in OpenAlex.

  1. Review
  2. β-Adrenergic Receptors: Not Always Outside-In.Physiology (Bethesda, Md.) · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. A cellular atlas of calcineurin signaling.Biochimica et biophysica acta. Molecular cell research · 2023
    Review
  11. A perinuclear calcium compartment regulates cardiac myocyte hypertrophy.Journal of molecular and cellular cardiology · 2022
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. CaMKIIδC Drives Early Adaptive CaCirculation research · 2020
    Article
  17. Article
  18. 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

4 authors at 2 institutions in 1 country.

Kimberly Dodge-KafkaCalhoun Center for Cardiology, Cardiac Signal Transduction and Cellular Biology Laboratory, University of Connecticut Health Center, Farmington, CT, USA. Electronic address: dodge@uchc.edu.
Moriah GildartCalhoun Center for Cardiology, Cardiac Signal Transduction and Cellular Biology Laboratory, University of Connecticut Health Center, Farmington, CT, USA.
Kristin TokarskiCalhoun Center for Cardiology, Cardiac Signal Transduction and Cellular Biology Laboratory, University of Connecticut Health Center, Farmington, CT, USA.
Michael S KapiloffDepartments of Ophthalmology and Medicine, Stanford Cardiovascular Institute, Stanford University, Palo Alto, CA, USA.
UConn Health · USCardiovascular Institute of the South · US

Funding

Stanford Vision Research CoreP30EY026877 · NEI · STANFORD UNIVERSITY · PI Jeffrey L Goldberg · 2017 to 2026
$8.0M
Function of MEF2 in Neuroprotection and Neuro-regeneration Following StrokeR01EY026766 · NEI · STANFORD UNIVERSITY · PI GOLDBERG, JEFFREY L, KAPILOFF, MICHAEL SETH · 2016 to 2020
$2.4M
Regulation of Histone Deacetylases by mAKAP SignalosomesR01HL146111 · NHLBI · STANFORD UNIVERSITY · PI DODGE-KAFKA, KIMBERLY L, KAPILOFF, MICHAEL SETH · 2019 to 2022
$2.2M
The Role of Perinuclear Calcium for The induction of Cardiac HypertrophyR01HL126825 · NHLBI · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI DODGE-KAFKA, KIMBERLY L, KAPILOFF, MICHAEL SETH · 2016 to 2019
$1.7M
Role of the F-Bar Protein CIP4 in Cardiac HypertrophyR01HL126950 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI KAPILOFF, MICHAEL SETH · 2016 to 2019
$1.6M
NEI NIH HHS P30 EY026877NEI NIH HHS R01 EY026766NHLBI NIH HHS R01 HL126825NHLBI NIH HHS R01 HL126950NHLBI NIH HHS R01 HL146111
6 · The paper itself

Abstract

Striated myocytes compose about half of the cells of the heart, while contributing the majority of the heart's mass and volume. In response to increased demands for pumping power, including in diseases of pressure and volume overload, the contractile myocytes undergo non-mitotic growth, resulting in increased heart mass, i.e. cardiac hypertrophy. Myocyte hypertrophy is induced by a change in the gene expression program driven by the altered activity of transcription factors and co-repressor and co-activator chromatin-associated proteins. These gene regulatory proteins are subject to diverse post-translational modifications and serve as nuclear effectors for intracellular signal transduction pathways, including those controlled by cyclic nucleotides and calcium ion. Scaffold proteins contribute to the underlying architecture of intracellular signaling networks by targeting signaling enzymes to discrete intracellular compartments, providing specificity to the regulation of downstream effectors, including those regulating gene expression. Muscle A-kinase anchoring protein β (mAKAPβ) is a well-characterized scaffold protein that contributes to the regulation of pathological cardiac hypertrophy. In this review, we discuss the mechanisms how this prototypical scaffold protein organizes signalosomes responsible for the regulation of class IIa histone deacetylases and cardiac transcription factors such as NFAT, MEF2, and HIF-1α, as well as how this signalosome represents a novel therapeutic target for the prevention or treatment of heart failure.

Indexed as

Ventricular RemodelingA Kinase Anchor ProteinsAnimalsCardiomegalyCell LineHistone DeacetylasesHumansMiceMyocytes, CardiacTranscription FactorsA Kinase Anchor ProteinsHistone DeacetylasesTranscription FactorsAKAPcAMPCardiac hypertrophyGene transcriptionKinase

Identifiers

PMID31299211
PMCPMC7197268
OpenAlexW2962305110

What OpenQuestion holds

Textmetadata
LicenceTDM
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.