The DOI matches its Crossref record.
A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutation
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Decreasing prelamin A or progerin levels delays the onset of progeroid features and extends lifespan in mouse models of HGPS.
“The causal relevance of nuclear lamina abnormalities in premature aging has been supported by the observation that decreasing prelamin A or progerin levels delays the onset of progeroid features and extends lifespan in mouse models of HGPS.”
From The Hallmarks of Aging (2013) · cites this paper as Yang et al., 2006
The Results (page unavailable) show that mice with one progerin-producing allele developed features later and survived longer than mice with two; FTI treatment also improved several disease features. But the paper does not show that experimentally decreasing prelamin A or progerin protein levels delayed onset or extended lifespan, and it does not report a survival benefit from FTI treatment. (LLM, conf=0.84)
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
No references could be resolved yet.
Research works printed but not linked: 8
- Goldman, R.D., et al. 2004. Accumulation of mutant lamin A causes progressive changes in nuclear archi- tecture in Hutchinson-Gilford progeria syndrome. Proc. Natl. Acad. Sci. U. S. A. 101:8963-8968.
- Yang, S.H., et al. 2005. Blocking protein farnesyl- transferase improves nuclear blebbing in mouse fibroblasts with a targeted Hutchinson-Gilford progeria syndrome mutation. Proc. Natl. Acad. Sci.
- Toth, J.I., et al. 2005. Blocking protein farnesyl- transferase improves nuclear shape in fibroblasts from humans with progeroid syndromes. Proc. Natl. Acad. Sci. U. S. A. 102:12873-12878.
- Mallampalli, M.P., Huyer, G., Bendale, P., Gelb, M.H., and Michaelis, S. 2005. Inhibiting farne- sylation reverses the nuclear morphology defect in a HeLa cell model for Hutchinson-Gilford progeria syndrome. Proc. Natl. Acad. Sci. U. S. A. 102:14416-14421.
- Capell, B.C., et al. 2005. Inhibiting farnesylation of progerin prevents the characteristic nuclear bleb- bing of Hutchinson-Gilford progeria syndrome. Proc. Natl. Acad. Sci. U. S. A. 102:12879-12884.
- Bergo, M.O., et al. 2002. Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect. Proc. Natl. Acad. Sci. U. S. A. 99:13049-13054.
- Fong, L.G., et al. 2004. Heterozygosity for Lmna defi- ciency eliminates the progeria-like phenotypes in Zmpste24-deficient mice. Proc. Natl. Acad. Sci. U. S. A. 101:18111-18116.
- Varga, R., et al. 2006. Progressive vascular smooth muscle cell defects in a mouse model of Hutchin- son-Gilford progeria syndrome. Proc. Natl. Acad. Sci.
Cited by
Sorted by citations
López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013) · Cell · doi:10.1016/j.cell.2013.05.039 · Cited by 14,982
Inflammation and aging: signaling pathways and intervention therapies
Li, X., Li, C., Zhang, W., Wang, Y., Qian, P., & Huang, H. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01502-8 · Cited by 1,443
Splicing-directed therapy in a new mouse model of human accelerated aging
Osorio, F. G., Navarro, C. L., Cadiñanos, J., López-Mejía, I. C., Quirós, P. M., Bartoli, C., Rivera, J., Tazi, J., Guzmán, G., Varela, I., et al. (2011) · Science Translational Medicine · doi:10.1126/scitranslmed.3002847 · Cited by 432
Hutchinson-Gilford Progeria Syndrome: A premature aging disease caused by LMNA gene mutations
Gonzalo, S., Kreienkamp, R., & Askjaer, P. (2017) · Ageing Research Reviews · doi:10.1016/j.arr.2016.06.007 · Cited by 324
Animal models of aging research: implications for human aging and age-related diseases
Mitchell, S. J., Scheibye-Knudsen, M., Longo, D. L., & de Cabo, R. (2015) · Annual Review of Animal Biosciences · doi:10.1146/annurev-animal-022114-110829 · Cited by 328
Werner and Hutchinson–Gilford progeria syndromes: mechanistic basis of human progeroid diseases
Kudlow, B. A., Kennedy, B. K., & Monnat, R. J. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2161 · Cited by 304
The hallmarks of fibroblast ageing
Tigges, J., Krutmann, J., Fritsche, E., Haendeler, J., Schaal, H., Fischer, J. W., Kalfalah, F., Reinke, H., Reifenberger, G., Stühler, K., et al. (2014) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2014.03.004 · Cited by 250
Aging Hallmarks: The Benefits of Physical Exercise
Rebelo-Marques, A., De Sousa Lages, A., Andrade, R., Ribeiro, C. F., Mota-Pinto, A., Carrilho, F., & Espregueira-Mendes, J. (2018) · Frontiers in Endocrinology · doi:10.3389/fendo.2018.00258 · Cited by 246
Hamczyk, M. R., Villa-Bellosta, R., Gonzalo, P., Andrés-Manzano, M. J., Nogales, P., Bentzon, J. F., López-Otín, C., & Andrés, V. (2018) · Circulation · doi:10.1161/circulationaha.117.030856 · Cited by 153
Mechanisms of cardiovascular disease in accelerated aging syndromes
Capell, B. C., Collins, F. S., & Nabel, E. G. (2007) · Circulation Research · doi:10.1161/circresaha.107.153692 · Cited by 134
Mouse Models to Disentangle the Hallmarks of Human Aging
Folgueras, A. R., Freitas-Rodríguez, S., Velasco, G., & López-Otín, C. (2018) · Circulation Research · doi:10.1161/circresaha.118.312204 · Cited by 113
Pereira, S., Bourgeois, P., Navarro, C., Esteves-Vieira, V., Cau, P., De Sandre-Giovannoli, A., & Lévy, N. (2008) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2008.04.003 · Cited by 85
Genomic instability and DNA replication defects in progeroid syndromes
Burla, R., La Torre, M., Merigliano, C., Vernì, F., & Saggio, I. (2018) · Nucleus · doi:10.1080/19491034.2018.1476793 · Cited by 59
Metabolic Dysfunction in Hutchinson–Gilford Progeria Syndrome
Kreienkamp, R., & Gonzalo, S. (2020) · Cells · doi:10.3390/cells9020395 · Cited by 45
Metadata
- Authors
- Yang, S. H.
- Venue
- Journal of Clinical Investigation
- Published
- 2006-08-01
- Volume
- 116
- Issue
- 8
- Pages
- 2115-2121
- ISSN
- 0021-9738
- Cited by
- 263
- References
- 0
- Language
- en
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
