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The Interplay of Protein Kinase A and Perilipin 5 Regulates Cardiac Lipolysis*♦

Overview of attention for article published in Journal of Biological Chemistry, November 2014
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  • Good Attention Score compared to outputs of the same age (76th percentile)
  • Good Attention Score compared to outputs of the same age and source (76th percentile)

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Article details
Title
The Interplay of Protein Kinase A and Perilipin 5 Regulates Cardiac Lipolysis*♦
Published in
Journal of Biological Chemistry, November 2014
DOI 10.1074/jbc.m114.604744
Pubmed ID
Authors
Abstract

Defective lipolysis in mice lacking adipose triglyceride lipase (ATGL) provokes severe cardiac steatosis and heart dysfunction, markedly shortening lifespan. Similarly, cardiac muscle (CM)-specific Plin5 overexpression (CM-Plin5) leads to severe triglyceride (TG) accumulation in cardiomyocytes via impairing TG breakdown. Interestingly, cardiac steatosis due to overexpression of Plin5 is compatible with normal heart function and lifespan indicating a more moderate impact of Plin5-overexpression on cardiac lipolysis and energy metabolism. We hypothesized that cardiac Plin5-overexpression does not constantly impair cardiac lipolysis. In line with this assumption, TG levels decreased in CM of fasted compared to non-fasted CM-Plin5 mice indicating that fasting may lead to a diminished barrier function of Plin5. Recent studies demonstrated that Plin5 is phosphorylated and activation of adenylyl cyclase leads to phosphorylation of Plin5, suggesting that Plin5 is a substrate for PKA. Furthermore, any significance of Plin5 phosphorylation by PKA in the regulation of TG mobilization from lipid droplets (LDs) is unknown. Here we show that the lipolytic barrier of Plin5-enriched LDs, either prepared from cardiac tissue of CM-Plin5 mice or Plin5-transfected cells, is abrogated by incubation with PKA. Notably, PKA-induced lipolysis of LDs enriched with Plin5 carrying a single mutation at serine 155 (PlinS155A) of the putative PKA phosphorylation site was substantially impaired revealing a critical role for PKA in Plin5-regulated lipolysis. The strong increase in protein levels of phosphorylated PKA in CM of Plin5 transgenic mice may partially restore fatty acid release from Plin5-enriched LDs, rendering these hearts compatible with normal heart function despite massive steatosis.

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Mendeley demographics

Mendeley demographics

The data shown below were compiled from readership statistics for 86 Mendeley readers of this research output. Click here to see the associated Mendeley record.
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Geographical breakdown

Geographical breakdown
Country Count As %
Finland 1 1%
China 1 1%
Austria 1 1%
Unknown 83 97%

Demographic breakdown

Readers by professional status
Readers by professional status Count As %
Student > Ph. D. Student 19 22%
Researcher 15 17%
Student > Master 9 10%
Student > Bachelor 6 7%
Professor > Associate Professor 5 6%
Other 15 17%
Unknown 17 20%
Readers by discipline
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 28 33%
Agricultural and Biological Sciences 14 16%
Medicine and Dentistry 9 10%
Pharmacology, Toxicology and Pharmaceutical Science 4 5%
Sports and Recreations 2 2%
Other 4 5%
Unknown 25 29%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 5. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 19 January 2015.
All research outputs
#6,754,036
of 25,374,647 outputs
Outputs from Journal of Biological Chemistry
#28,717
of 85,241 outputs
Outputs of similar age
#84,946
of 368,584 outputs
Outputs of similar age from Journal of Biological Chemistry
#116
of 492 outputs
Altmetric has tracked 25,374,647 research outputs across all sources so far. This one has received more attention than most of these and is in the 73rd percentile.
So far Altmetric has tracked 85,241 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.1. This one has gotten more attention than average, scoring higher than 66% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 368,584 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 76% of its contemporaries.
We're also able to compare this research output to 492 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 76% of its contemporaries.