Lamin A/C deficiency causes defective nuclear mechanics and mechanotransduction.

By J. Lammerding, P. C. Schulze, Tomosaburo Takahashi, S. Kozlov, Teresa L. Sullivan, Roger D. Kamm, C. Stewart, Richard T Lee. Journal of Clinical Investigation, 2004

1,048 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f6047eb3c66af00d6c9847373325dbb50f4ec0a1

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. Peter C. Searson
2. Donald E. Ingber
3. Christopher S. Chen
4. Denis Wirtz
5. T. Mammoto
6. Carmel Majidi

Citations in the corpus

• The physics of cancer: the role of physical interactions and mechanical forces in metastasis (2011, neutral): “Indeed, depletion of LINC complex components, including nesprins and SUN proteins, leads to nuclear shape defects and an associated softening of the nucleus and the cytoplas”
• A perinuclear actin cap regulates nuclear shape (2009, background): “Actin cap-nucleus connections are altered in cells from mouse models of muscular dystrophy and progeria (17, 24, 25), which disorganizes the actin cap and may explain the deformed shape of the nucleus in these diseased cells.”
• Cellular mechanotransduction: putting all the pieces together again (2006, background): “Severe muscular dystrophies and cardiac myopathies similarly result from mutations of ECM molecules, integrins, adhesion molecules, cytoskeletal proteins or nuclear lamins that form the structural scaffolds that mediate force channeling in muscle (119, 155).”
• Mechanical control of stem cell differentiation (2008, background): “, 2007), the nuclear lamina or nuclear deformations (Lammerding et al., 2004; Lammerding et al., 2005), and primary cilia (Resnick and Hopfer, 2007).”
• The nuclear lamina comes of age (2005, background): “Interestingly, loss of A-type lamins causes both mechanical weakness and defects in mechanical-stress-dependent gene expression in vivo”
• "Laminopathies": a wide spectrum of human diseases. (2007, background): “Further support for this as a possible pathogenic mechanism comes from the observations that fibroblasts from Lmna null mice have defects in nuclear mechanics and mechanotransduction [97,98].”
• Mechanical control of tissue and organ development (2010, background): “This could be relevant for developmental control because nuclear envelope lamins stabilize nuclear architecture under mechanical strain through mechanically activated NF-kB transcription (Lammerding et al., 2004).”
• Mechanotransduction gone awry (2009, background): “Cells from these animals are characterized by decreased nuclear stiffness, increased nuclear fragility and impaired activation of mechanosensitive genes, causing decreased viability in cells subjected to repetitive strai”
• Dilated Cardiomyopathy: Genetic Determinants and Mechanisms (2017, neutral): “Loss of LMNA leads to a defect in mechanosignaling.(93,94)”
• Mechanotransduction at a distance: mechanically coupling the extracellular matrix with the nucleus (2009, background): “Cells that are deficient for A-type lamins have decreased viability, reduced expression of mechanosensitive genes and altered nuclear mechanics in response to mechanical distortion, whereas defects in lamin B1 do not produce similar effects, which suggests that the A-type lamins might have a more ce”