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Genetic disruption of Ano5 in mice does not recapitulate human ANO5-deficient muscular dystrophy

Overview of attention for article published in Skeletal Muscle, December 2015
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About this Attention Score

  • Above-average Attention Score compared to outputs of the same age (61st percentile)

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3 tweeters

Citations

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31 Dimensions

Readers on

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30 Mendeley
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Title
Genetic disruption of Ano5 in mice does not recapitulate human ANO5-deficient muscular dystrophy
Published in
Skeletal Muscle, December 2015
DOI 10.1186/s13395-015-0069-z
Pubmed ID
Authors

Jing Xu, Mona El Refaey, Li Xu, Lixia Zhao, Yandi Gao, Kyle Floyd, Tallib Karaze, Paul M. L. Janssen, Renzhi Han

Abstract

Anoctamin 5 (ANO5) is a member of a conserved gene family (TMEM16), which codes for proteins predicted to have eight transmembrane domains and putative Ca(2+)-activated chloride channel (CaCC) activity. It was recently reported that mutations in this gene result in the development of limb girdle muscular dystrophy type 2L (LGMD2L), Miyoshi myopathy type 3 (MMD3), or gnathodiaphyseal dysplasia 1 (GDD1). Currently, there is a lack of animal models for the study of the physiological function of Ano5 and the disease pathology in its absence. Here, we report the generation and characterization of the first Ano5-knockout (KO) mice. Our data demonstrate that the KO mice did not present overt skeletal or cardiac muscle pathology at rest conditions from birth up to 18 months of age. There were no significant differences in force production or force deficit following repeated eccentric contractions between wild type (WT) and KO mice. Although cardiac hypertrophy developed similarly in both KO and WT mice after daily isoproterenol (ISO, 100 mg/kg) treatment via intraperitoneal injection for 2 weeks, they were functionally indiscernible. However, microarray analysis identified the genes involved in lipid metabolism, and complement pathways were altered in the KO skeletal muscle. Taken together, these data provide the evidence to show that genetic ablation of Ano5 in C57BL/6J mice does not cause overt pathology in skeletal and cardiac muscles, but Ano5 deficiency may lead to altered lipid metabolism and inflammation signaling.

Twitter Demographics

The data shown below were collected from the profiles of 3 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 30 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Germany 2 7%
Japan 1 3%
Unknown 27 90%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 7 23%
Student > Master 5 17%
Student > Bachelor 3 10%
Student > Doctoral Student 2 7%
Researcher 2 7%
Other 7 23%
Unknown 4 13%
Readers by discipline Count As %
Agricultural and Biological Sciences 10 33%
Biochemistry, Genetics and Molecular Biology 7 23%
Medicine and Dentistry 4 13%
Sports and Recreations 2 7%
Pharmacology, Toxicology and Pharmaceutical Science 1 3%
Other 0 0%
Unknown 6 20%

Attention Score in Context

This research output has an Altmetric Attention Score of 2. 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 15 February 2016.
All research outputs
#2,909,380
of 7,196,678 outputs
Outputs from Skeletal Muscle
#122
of 168 outputs
Outputs of similar age
#109,771
of 300,135 outputs
Outputs of similar age from Skeletal Muscle
#12
of 15 outputs
Altmetric has tracked 7,196,678 research outputs across all sources so far. This one has received more attention than most of these and is in the 58th percentile.
So far Altmetric has tracked 168 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.0. This one is in the 23rd percentile – i.e., 23% of its peers scored the same or lower than it.
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 300,135 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 61% of its contemporaries.
We're also able to compare this research output to 15 others from the same source and published within six weeks on either side of this one. This one is in the 13th percentile – i.e., 13% of its contemporaries scored the same or lower than it.