Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
Volume 1781, Issue 1-2, Pages 36-39Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbalip.2007.11.003
Keywords
progeria; aging; protein farnesyltransferase inhibitor; knock-in mice
Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL086683, R01HL076839] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR050200] Funding Source: NIH RePORTER
- NHLBI NIH HHS [R01 HL076839-03, HL86683, R01 HL086683, R01 HL076839-02, HL76839, R01 HL076839-01A1, R01 HL076839] Funding Source: Medline
- NIAMS NIH HHS [R01 AR050200-04, AR050200, R01 AR050200, R01 AR050200-02, R01 AR050200-01, R01 AR050200-02S1, R01 AR050200-06, R01 AR050200-03, R01 AR050200-05] Funding Source: Medline
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Hutchinson-Gilford progeria syndrome (HGPS) is a progeroid syndrome characterized by multiple aging-like disease phenotypes. We recently reported that a protein farnesyltransferase inhibitor (FTI) improved several disease phenotypes in mice with a HGPS mutation (Lmna(HG/+)). Here, we investigated the impact of an FTI on the survival of Lmna(HG/+) mice. The FTI significantly improved the survival of both male and female Lmna(HG/+) mice. Treatment with the FTI also improved body weight curves and reduced the number of spontaneous rib fractures. This study provides further evidence for a beneficial effect of an FTI in HGPS. (c) 2007 Elsevier B.V. All rights reserved.
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