The farnesyl transferase inhibitor (FTI) lonafarnib improves nuclear morphology in ZMPSTE24-deficient fibroblasts from patients with the progeroid disorder MAD-B

Kamsi O. Odinammadua Department of Cell Biology, The Johns Hopkins School of Medicine, Baltimore, MD, USA

https://orcid.org/0000-0003-0243-2395 View further author information

Khurts Shilagardia Department of Cell Biology, The Johns Hopkins School of Medicine, Baltimore, MD, USAView further author information

Kelsey Tuminellib The Progeria Research Foundation, Peabody, MA, USAView further author information

Daniel P. Judgec Department of Medicine, Medical University of South Carolina, Charleston, SC, USAView further author information

Leslie B. Gordonb The Progeria Research Foundation, Peabody, MA, USA;d Department of Anesthesiology, Critical Care and Pain Medicine, Boston Children’s Hospital and Harvard Medical School, Boston, MA, USA;e Department of Pediatrics, Division of Genetics, Hasbro Children’s Hospital and Warren Alpert Medical School of Brown University, Providence, RI, USAView further author information

Susan Michaelisa Department of Cell Biology, The Johns Hopkins School of Medicine, Baltimore, MD, USACorrespondence[email protected]
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The farnesyl transferase inhibitor (FTI) lonafarnib improves nuclear morphology in ZMPSTE24-deficient fibroblasts from patients with the progeroid disorder MAD-B

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The farnesyl transferase inhibitor (FTI) lonafarnib improves nuclear morphology in ZMPSTE24-deficient fibroblasts from patients with the progeroid disorder MAD-B

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