Abstract
Analysis of nuclear actin in human progeria cells
Highlights
In Hutchinson-Gilford progeria syndrome (HGPS) cells, several nuclear defects are observed such as irregular nuclear shape and increased DNA damage
Since progerin lacks actin binding sites [1], we hypothesized that the expression of progerin impairs functions and dynamics of nuclear actin, and that these nuclear actin dysfunctions are relevant to HGPS phenotypes
When we observed nuclear F-actin, we found that the HGPS cells contains less nuclear F-actin as compared to control cells, in which progerin expression is not induced
Summary
1. Solarczyk, K.J. et al Inducing local DNA damage by visible light to study chromatin repair. Analysis of nuclear actin in human progeria cells. Yuto Takahashi1, Nanako Machida1, Tom Misteli2, Robert Grosse3, Kei Miyamoto4, Masahiko Harata1. 1 Graduated School of Agricultural Science, Tohoku University, Japan; 2 National Cancer Institute, National Institutes of Health, USA; 3 Institute of Pharmacology, BPC University of Marburg, Germany; 4 Faculty of Biology-Oriented Science and Technology, Kinki University, Japan. Hutchinson-Gilford progeria syndrome (HGPS) is a rare premature disorder caused by de novo single base substitution in the lamin A gene.
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