Associated Papers
Stem cell-associated osteogenic deficiency causes craniofacial deformities with progeroid accumulation of prelamin A.
Li K et al.
Jci Insight, 2026
Prelamin A Does Not Promote Atherosclerosis or Vascular Smooth Muscle Loss.
Wang Y et al.
Biorxiv : the Preprint Server for Biology, 2025
The Accumulation of Progerin Underlies the Loss of Aortic Smooth Muscle Cells in Hutchinson-Gilford Progeria Syndrome.
Kim PH et al.
Biorxiv : the Preprint Server for Biology, 2024
Defective prelamin A processing promotes unconventional necroptosis driven by nuclear RIPK1.
Yang Y et al.
Nature Cell Biology, 2024
Prelamin A and ZMPSTE24 in premature and physiological aging.
Worman HJ et al.
Nucleus (austin, Tex.), 2023
The farnesyl transferase inhibitor (FTI) lonafarnib improves nuclear morphology in ZMPSTE24-deficient fibroblasts from patients with the progeroid disorder MAD-B.
Odinammadu KO et al.
Nucleus (austin, Tex.), 2023
Abolishing the prelamin A ZMPSTE24 cleavage site leads to progeroid phenotypes with near-normal longevity in mice.
Wang Y et al.
Proceedings of the National Academy of Sciences of the United States of America, 2022
Requirements for efficient proteolytic cleavage of prelamin A by ZMPSTE24.
Barrowman J et al.
Plos One, 2012
Muscular laminopathies: role of prelamin A in early steps of muscle differentiation.
Maraldi NM et al.
Advances in Enzyme Regulation, 2011
Altered pre-lamin A processing is a common mechanism leading to lipodystrophy.
Capanni C et al.
Human Molecular Genetics, 2005
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