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Sustained accumulation of prelamin A and depletion of lamin A/C both cause oxidative stress and mitochondrial dysfunction but induce different cell fates
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Multiplexed profiling of secreted proteins for the detection of potential space biomarkers
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Repetitive disruptions of the nuclear envelope invoke temporary loss of cellular compartmentalization in laminopathies
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Increased plasticity of the nuclear envelope and hypermobility of telomeres due to the loss of A-type lamins