ArticleMolecular biology of the cell2014
A pathway linking oxidative stress and the Ran GTPase system in progeria.
Article in Molecular biology of the cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Nucleus softens during herpesvirus infection.PLoS pathogens · 2026Article
- Nuclear pore and nucleocytoplasmic transport impairment in oxidative stress-induced neurodegeneration: relevance to molecular mechanisms in Pathogenesis of Parkinson's and other related neurodegenerative diseases.Molecular neurodegeneration · 2024Review
- The syntaxin-binding protein STXBP5 regulates progerin expression.Scientific reports · 2024Article
- Thermal Stress and Nuclear Transport.Advances in experimental medicine and biology · 2024Review
- Article
- Progerin-expressing endothelial cells are unable to adapt to shear stress.Biophysical journal · 2022Article
- Disruption of nucleocytoplasmic trafficking as a cellular senescence driver.Experimental & molecular medicine · 2021Article
- Local translation in nuclear condensate amyloid bodies.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Lamin microaggregates lead to altered mechanotransmission in progerin-expressing cells.Nucleus (Austin, Tex.) · 2020Article
- Article
- Thioredoxin-related transmembrane protein 2 (TMX2) regulates the Ran protein gradient and importin-β-dependent nuclear cargo transport.Scientific reports · 2019Article
- Enhanced nuclear protein export in premature aging and rescue of the progeria phenotype by modulation of CRM1 activity.Aging cell · 2019Article
- Fluorescence-based quantification of nucleocytoplasmic transport.Methods (San Diego, Calif.) · 2019Article
- Article
- Lamin A mutation impairs interaction with nucleoporin NUP155 and disrupts nucleocytoplasmic transport in atrial fibrillation.Human mutation · 2019Article
- A nuclear lamina-chromatin-Ran GTPase axis modulates nuclear import and DNA damage signaling.Aging cell · 2019Article
- Single-dose radiotherapy disables tumor cell homologous recombination via ischemia/reperfusion injury.The Journal of clinical investigation · 2019Article
- Impaired Nuclear Export of Polyglutamine-Expanded Androgen Receptor in Spinal and Bulbar Muscular Atrophy.Scientific reports · 2019Article
- Inhibition of the acetyltransferase NAT10 normalizes progeric and aging cells by rebalancing the Transportin-1 nuclear import pathway.Science signaling · 2018Article
- Nuclear transport adapts to varying heat stress in a multistep mechanism.The Journal of cell biology · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Maintaining the Ran GTPase at a proper concentration in the nucleus is important for nucleocytoplasmic transport. Previously we found that nuclear levels of Ran are reduced in cells from patients with Hutchinson-Gilford progeria syndrome (HGPS), a disease caused by constitutive attachment of a mutant form of lamin A (termed progerin) to the nuclear membrane. Here we explore the relationship between progerin, the Ran GTPase, and oxidative stress. Stable attachment of progerin to the nuclear membrane disrupts the Ran gradient and results in cytoplasmic localization of Ubc9, a Ran-dependent import cargo. Ran and Ubc9 disruption can be induced reversibly with H2O2. CHO cells preadapted to oxidative stress resist the effects of progerin on Ran and Ubc9. Given that HGPS-patient fibroblasts display elevated ROS, these data suggest that progerin inhibits nuclear transport via oxidative stress. A drug that inhibits pre-lamin A cleavage mimics the effects of progerin by disrupting the Ran gradient, but the effects on Ran are observed before a substantial ROS increase. Moreover, reducing the nuclear concentration of Ran is sufficient to induce ROS irrespective of progerin. We speculate that oxidative stress caused by progerin may occur upstream or downstream of Ran, depending on the cell type and physiological setting.
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