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Cited by 553

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford progeria syndrome

Scaffidi, Paola, Misteli, Tom·2005·Nature Medicine
DOI 10.1038/nm1204
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Crossref · 10.1038/nm1204

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1 of 1 references verified0 citation errors · 0 not checkable

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  • LAKI mice carry a G609G mutation in Lmna, leading to accumulation of a truncated lamin A (progerin), which is responsible for human HGPS.

    “We chose the premature aging mouse model that carries a G609G mutation in the gene Lmna (LAKI).This mutation leads to the accumulation of a truncated form of lamin A (called progerin), which is responsible for human HGPS”

    From In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming. (2016) · cites this paper as Scaffidi and Misteli, 2005

    The passage labeled Abstract (page unavailable) says that the human HGPS-associated LMNA G608G mutation produces truncated lamin A, supporting the disease mechanism. It does not identify LAKI mice or a G609G mutation; its discussion of a mouse model instead describes an L530P mutation. Thus it does not support the claim about the chosen mouse model. (LLM, conf=0.90)

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Citations

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Research works printed but not linked: 21

  1. DeBusk, F.L. The Hutchinson-Gilford progeria syndrome. Report of 4 cases and review of the literature. J. Pediatr. 80, 697–724 (1972). · DOI
  2. Uitto, J. Searching for clues to premature aging. Trends Endocrinol. Metab. 13, 140–141 (2002). · DOI
  3. Eriksson, M. et al. Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome. Nature 423, 293–298 (2003). · DOI · Paper page
  4. De Sandre-Giovannoli, A. et al. Lamin A truncation in Hutchinson-Gilford progeria. Science 300, 2055 (2003). · DOI · Paper page
  5. Csoka, A.B. et al. Novel lamin A/C gene (LMNA) mutations in atypical progeroid syndromes. J. Med. Genet. 41, 304–308 (2004). · DOI
  6. Goldman, R.D. et al. Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome. Proc. Natl. Acad. Sci. USA 101, 8963–8968 (2004). · DOI · Paper page
  7. Ye, Q., Callebaut, I., Pezhman, A., Courvalin, J.C. & Worman, H.J. Domain-specific interactions of human HP1-type chromodomain proteins and inner nuclear membrane protein LBR. J. Biol. Chem. 272, 14983–14989 (1997). · DOI
  8. Jenuwein, T. & Allis, C.D. Translating the histone code. Science 293, 1074–1080 (2001). · DOI · Paper page
  9. Holt, I. et al. Effect of pathogenic mis-sense mutations in lamin A on its interaction with emerin in vivo. J. Cell Sci. 116, 3027–3035 (2003). · DOI
  10. Vaughan, A. et al. Both emerin and lamin C depend on lamin A for localization at the nuclear envelope. J. Cell Sci. 114, 2577–2590 (2001). · DOI
  11. Johnson, B.R. et al. A-type lamins regulate retinoblastoma protein function by promoting subnuclear localization and preventing proteasomal degradation. Proc. Natl. Acad. Sci. USA 101, 9677–9682 (2004). · DOI
  12. Sazani, P. & Kole, R. Therapeutic potential of antisense oligonucleotides as modulators of alternative splicing. J. Clin. Invest. 112, 481–486 (2003). · DOI
  13. Giles, R.V., Spiller, D.G., Clark, R.E. & Tidd, D.M. Antisense morpholino oligonucleotide analog induces missplicing of C-myc mRNA. Antisense Nucleic Acid Drug Dev. 9, 213–220 (1999). · DOI
  14. Summerton, J. Morpholino antisense oligomers: the case for an RNase H-independent structural type. Biochim. Biophys. Acta 1489, 141–158 (1999). · DOI
  15. Lin, F. & Worman, H.J. Structural organization of the human gene encoding nuclear lamin A and nuclear lamin C. J. Biol. Chem. 268, 16321–16326 (1993). · DOI
  16. Summerton, J. et al. Morpholino and phosphorothioate antisense oligomers compared in cell-free and in-cell systems. Antisense Nucleic Acid Drug Dev. 7, 63–70 (1997). · DOI
  17. Ly, D.H., Lockhart, D.J., Lerner, R.A. & Schultz, P.G. Mitotic misregulation and human aging. Science 287, 2486–2492 (2000). · DOI · Paper page
  18. Csoka, A.B. et al. Genome-scale expression profiling of Hutchinson-Gilford progeria syndrome reveals widespread transcriptional misregulation leading to mesodermal/mesenchymal defects and accelerated atherosclerosis. Aging Cell 3, 235–243 (2004). · DOI
  19. Mounkes, L.C., Kozlov, S., Hernandez, L., Sullivan, T. & Stewart, C.L. A progeroid syndrome in mice is caused by defects in A-type lamins. Nature 423, 298–301 (2003). · DOI
  20. Moulton, H.M., Nelson, M.H., Hatlevig, S.A., Reddy, M.T. & Iversen, P.L. Cellular uptake of antisense morpholino oligomers conjugated to arginine-rich peptides. Bioconjug. Chem. 15, 290–299 (2004). · DOI
  21. Gebski, B.L., Mann, C.J., Fletcher, S. & Wilton, S.D. Morpholino antisense oligonucleotide induced dystrophin exon 23 skipping in mdx mouse muscle. Hum. Mol. Genet. 12, 1801–1811 (2003). · DOI

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Metadata

Authors
Scaffidi, P., & Misteli, T.
Venue
Nature Medicine
Publisher
Springer Science and Business Media LLC
Published
2005-03-06
Volume
11
Issue
4
Pages
440-445
ISSN
  • 1078-8956
  • 1546-170X
DOI
10.1038/nm1204
Cited by
553
References
1
Language
en
Licence
www.springer.com/tdm (tdm)

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