Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford progeria syndrome
- 6 March 2005
- journal article
- research article
- Published by Springer Science and Business Media LLC in Nature Medicine
- Vol. 11 (4), 440-445
- https://doi.org/10.1038/nm1204
Abstract
No abstract availableKeywords
This publication has 22 references indexed in Scilit:
- Genome‐scale expression profiling of Hutchinson–Gilford progeria syndrome reveals widespread transcriptional misregulation leading to mesodermal/mesenchymal defects and accelerated atherosclerosisAging Cell, 2004
- Novel lamin A/C gene (LMNA) mutations in atypical progeroid syndromesJournal of Medical Genetics, 2004
- Cellular Uptake of Antisense Morpholino Oligomers Conjugated to Arginine-Rich PeptidesBioconjugate Chemistry, 2004
- Effect of pathogenic mis-sense mutations in lamin A on its interaction with emerin in vivoJournal of Cell Science, 2003
- A progeroid syndrome in mice is caused by defects in A-type laminsNature, 2003
- Translating the Histone CodeScience, 2001
- Mitotic Misregulation and Human AgingScience, 2000
- Antisense Morpholino Oligonucleotide Analog Induces Missplicing of C-mycmRNAAntisense and Nucleic Acid Drug Development, 1999
- Morpholino and Phosphorothioate Antisense Oligomers Compared in Cell-Free and In-Cell SystemsAntisense and Nucleic Acid Drug Development, 1997
- The Hutchinson-Gilford progeria syndrome: Report of 4 cases and review of the literatureThe Journal of Pediatrics, 1972