ATM Modulates Nuclear Mechanics by Regulating Lamin A Levels.

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作者： Pragya,Shah ^[1] ; Connor W,McGuigan ^[1] ; Svea,Cheng ^[1] ; Claire,Vanpouille-Box ^[2] ; Sandra,Demaria ^[3] ; Robert S,Weiss ^[4] ; Jan,Lammerding ^[5]

作者单位： Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, United States. ^[1] Department of Radiation Oncology, Weill Cornell Medicine, New York City, NY, United States. ^[2] Department of Radiation Oncology, Weill Cornell Medicine, New York City, NY, United States.;Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York City, NY, United States. ^[3] Department of Biomedical Sciences, Cornell University, Ithaca, NY, United States. ^[4] Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY, United States.;Nancy E. and Peter C. Meinig School of Biomedical Engineering, Cornell University, Ithaca, NY, United States. ^[5]

关键词 ATM ataxia-telangiectasia (AT)cancer biology cell migration confined migration lamin (A/C)mechanobiology nuclear mechanics

DOI 10.3389/fcell.2022.875132

PMID 35721517

发布时间 2024-08-29

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Frontiers in cell and developmental biology

2022年10卷

875132页

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ATM Modulates Nuclear Mechanics by Regulating Lamin A Levels.

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ATM Modulates Nuclear Mechanics by Regulating Lamin A Levels.

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