↓ Skip to main content

RETRACTED ARTICLE: Transgenic mice overexpressing the ALS-linked protein Matrin 3 develop a profound muscle phenotype

Overview of attention for article published in Acta Neuropathologica Communications, November 2016
Altmetric Badge

About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • Among the highest-scoring outputs from this source (#33 of 559)
  • High Attention Score compared to outputs of the same age (89th percentile)
  • High Attention Score compared to outputs of the same age and source (87th percentile)

Mentioned by

news
1 news outlet
blogs
1 blog
twitter
4 tweeters
facebook
1 Facebook page

Citations

dimensions_citation
10 Dimensions

Readers on

mendeley
36 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
RETRACTED ARTICLE: Transgenic mice overexpressing the ALS-linked protein Matrin 3 develop a profound muscle phenotype
Published in
Acta Neuropathologica Communications, November 2016
DOI 10.1186/s40478-016-0393-5
Pubmed ID
Authors

Christina Moloney, Sruti Rayaprolu, John Howard, Susan Fromholt, Hilda Brown, Matt Collins, Mariela Cabrera, Colin Duffy, Zoe Siemienski, Dave Miller, Maurice S. Swanson, Lucia Notterpek, David R. Borchelt, Jada Lewis

Abstract

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder of upper and lower motor neurons. Mutations in the gene encoding the nuclear matrix protein Matrin 3 have been found in familial cases of ALS, as well as autosomal dominant distal myopathy with vocal cord and pharyngeal weakness. We previously found that spinal cord and muscle, organs involved in either ALS or distal myopathy, have relatively lower levels of Matrin 3 compared to the brain and other peripheral organs in the murine system. This suggests that these organs may be vulnerable to any changes in Matrin 3. In order to determine the role of Matrin 3 in these diseases, we created a transgenic mouse model for human wild-type Matrin 3 using the mouse prion promoter (MoPrP) on a FVB background.We identified three founder transgenic lines that produced offspring in which mice developed either hindlimb paresis or paralysis with hindlimb and forelimb muscle atrophy. Muscles of affected mice showed a striking increase in nuclear Matrin 3, as well as the presence of rounded fibers, vacuoles, nuclear chains, and subsarcolemmal nuclei. Immunoblot analysis of the gastrocnemius muscle from phenotypic mice showed increased levels of Matrin 3 products migrating at approximately 120 (doublet), 90, 70, and 55 kDa. While there was no significant change in the levels of Matrin 3 in the spinal cord in the phenotypic mice, the ventral horn contained individual cells with cytoplasmic redistribution of Matrin 3, as well as gliosis. The phenotypes of these mice indicate that dysregulation of Matrin 3 levels is deleterious to neuromuscular function.

Twitter Demographics

The data shown below were collected from the profiles of 4 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 36 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Australia 1 3%
Unknown 35 97%

Demographic breakdown

Readers by professional status Count As %
Student > Master 8 22%
Student > Ph. D. Student 7 19%
Researcher 3 8%
Student > Bachelor 2 6%
Student > Postgraduate 2 6%
Other 7 19%
Unknown 7 19%
Readers by discipline Count As %
Agricultural and Biological Sciences 7 19%
Biochemistry, Genetics and Molecular Biology 6 17%
Neuroscience 6 17%
Medicine and Dentistry 4 11%
Nursing and Health Professions 2 6%
Other 2 6%
Unknown 9 25%

Attention Score in Context

This research output has an Altmetric Attention Score of 17. 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 18 January 2018.
All research outputs
#819,142
of 12,384,832 outputs
Outputs from Acta Neuropathologica Communications
#33
of 559 outputs
Outputs of similar age
#35,833
of 349,527 outputs
Outputs of similar age from Acta Neuropathologica Communications
#3
of 24 outputs
Altmetric has tracked 12,384,832 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 93rd percentile: it's in the top 10% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 559 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.0. This one has done particularly well, scoring higher than 94% 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 349,527 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 89% of its contemporaries.
We're also able to compare this research output to 24 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 87% of its contemporaries.