Blocking protein farnesyltransferase improves nuclear shape in fibroblasts from humans with progeroid syndromes
Author:
Publisher
Proceedings of the National Academy of Sciences
Subject
Multidisciplinary
Reference23 articles.
1. Loss of ZMPSTE24 (FACE-1) causes autosomal recessive restrictive dermopathy and accumulation of Lamin A precursors
2. Recurrent de novo point mutations in lamin A cause Hutchinson–Gilford progeria syndrome
3. Edible vaccines: not quite ready for prime time
4. Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect
5. Life at the edge: the nuclear envelope and human disease
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1. TIPE2 gene transfer ameliorates aging-associated osteoarthritis in a progeria mouse model by reducing inflammation and cellular senescence;Molecular Therapy;2024-09
2. Progerin forms an abnormal meshwork and has a dominant-negative effect on the nuclear lamina;Proceedings of the National Academy of Sciences;2024-06-25
3. Differential Expression of LMNA/C and Insulin Receptor Transcript Variants in Peripheral Blood Mononuclear Cells of Leukemia Patients;Journal of Clinical Medicine;2024-04-27
4. Deciphering the role of neddylation in tumor microenvironment modulation: common outcome of multiple signaling pathways;Biomarker Research;2024-01-08
5. The farnesyl transferase inhibitor (FTI) lonafarnib improves nuclear morphology in ZMPSTE24-deficient fibroblasts from patients with the progeroid disorder MAD-B;Nucleus;2023-12-05
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