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Oxidative Stress Induces Nuclear-to-Cytosol Shift of hMSH3, a Potential Mechanism for EMAST in Colorectal Cancer Cells

Overview of attention for article published in PLOS ONE, November 2012
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Title
Oxidative Stress Induces Nuclear-to-Cytosol Shift of hMSH3, a Potential Mechanism for EMAST in Colorectal Cancer Cells
Published in
PLOS ONE, November 2012
DOI 10.1371/journal.pone.0050616
Pubmed ID
Authors

Stephanie S. Tseng-Rogenski, Heekyung Chung, Maike B. Wilk, Shuai Zhang, Moriya Iwaizumi, John M. Carethers

Abstract

Elevated microsatellite alterations at selected tetranucleotide repeats (EMAST) is a genetic signature observed in 60% of sporadic colorectal cancers (CRCs). Unlike microsatellite unstable CRCs where hypermethylation of the DNA mismatch repair (MMR) gene hMLH1's promoter is causal, the precise cause of EMAST is not clearly defined but points towards hMSH3 deficiency.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 23 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 23 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 6 26%
Researcher 5 22%
Student > Ph. D. Student 2 9%
Student > Bachelor 2 9%
Student > Doctoral Student 1 4%
Other 1 4%
Unknown 6 26%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 5 22%
Agricultural and Biological Sciences 4 17%
Immunology and Microbiology 2 9%
Pharmacology, Toxicology and Pharmaceutical Science 2 9%
Medicine and Dentistry 2 9%
Other 2 9%
Unknown 6 26%