ArticleCommunications biology2022
The transcription factor PREP1(PKNOX1) regulates nuclear stiffness, the expression of LINC complex proteins and mechanotransduction.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- NUAK1 Inhibition Alleviates Ischemia-Reperfusion Injury via SYNE1-YAP1.Circulation research · 2026Article
- Role of YAP/TAZ Mechanobiological Signaling in Osteoporosis and Osteoarthritis.Calcified tissue international · 2026Review
- Modulating cell surface chemistry through mild reduction reinforces extracellular-to-intracellular transmission forces and mechano-signaling.Materials today. Bio · 2026Article
- Stem Cell-Derived Organoids for Cancer Therapy: Precision Medicine and Drug Selection.International journal of molecular sciences · 2026Review
- Nuclear Mechanics and Nuclear Mechanotransduction in Cancer Cell Migration and Invasion.Biomolecules · 2026Review
- Cellular mechanosignaling for sensing and transducing matrix rigidity.Current opinion in cell biology · 2023Review
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Authors and funding
14 authors.
Funding
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Abstract
Mechanosignaling, initiated by extracellular forces and propagated through the intracellular cytoskeletal network, triggers signaling cascades employed in processes as embryogenesis, tissue maintenance and disease development. While signal transduction by transcription factors occurs downstream of cellular mechanosensing, little is known about the cell intrinsic mechanisms that can regulate mechanosignaling. Here we show that transcription factor PREP1 (PKNOX1) regulates the stiffness of the nucleus, the expression of LINC complex proteins and mechanotransduction of YAP-TAZ. PREP1 depletion upsets the nuclear membrane protein stoichiometry and renders nuclei soft. Intriguingly, these cells display fortified actomyosin network with bigger focal adhesion complexes resulting in greater traction forces at the substratum. Despite the high traction, YAP-TAZ translocation is impaired indicating disrupted mechanotransduction. Our data demonstrate mechanosignaling upstream of YAP-TAZ and suggest the existence of a transcriptional mechanism actively regulating nuclear membrane homeostasis and signal transduction through the active engagement/disengagement of the cell from the extracellular matrix.
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Registered trials
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