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Lamin A/C Haploinsufficiency Modulates the Differentiation Potential of Mouse Embryonic Stem Cells

Overview of attention for article published in PLOS ONE, February 2013
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Title
Lamin A/C Haploinsufficiency Modulates the Differentiation Potential of Mouse Embryonic Stem Cells
Published in
PLOS ONE, February 2013
DOI 10.1371/journal.pone.0057891
Pubmed ID
Authors

Poonam Sehgal, Pankaj Chaturvedi, R. Ileng Kumaran, Satish Kumar, Veena K. Parnaik

Abstract

Lamins are structural proteins that are the major determinants of nuclear architecture and play important roles in various nuclear functions including gene regulation and cell differentiation. Mutations in the human lamin A gene cause a spectrum of genetic diseases that affect specific tissues. Most available mouse models for laminopathies recapitulate disease symptoms for muscle diseases and progerias. However, loss of human lamin A/C also has highly deleterious effects on fetal development. Hence it is important to understand the impact of lamin A/C expression levels on embryonic differentiation pathways.

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Mendeley readers

The data shown below were compiled from readership statistics for 61 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 3 5%
United Kingdom 1 2%
Lebanon 1 2%
Portugal 1 2%
Unknown 55 90%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 19 31%
Researcher 9 15%
Student > Bachelor 6 10%
Student > Master 5 8%
Student > Doctoral Student 4 7%
Other 7 11%
Unknown 11 18%
Readers by discipline Count As %
Agricultural and Biological Sciences 24 39%
Biochemistry, Genetics and Molecular Biology 14 23%
Medicine and Dentistry 4 7%
Engineering 2 3%
Pharmacology, Toxicology and Pharmaceutical Science 1 2%
Other 5 8%
Unknown 11 18%