ArticleJournal of molecular biology2011
Nonlinear viscoelasticity of actin transiently cross-linked with mutant α-actinin-4.
Article in Journal of molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 47 citations in OpenAlex.
- Bound water as a kinetic crosslinker for bio-inspired impact-stiffening polymers.Nature communications · 2026Article
- State-dependent energy conversion produces degenerate dissipation in active actomyosin networks.bioRxiv : the preprint server for biology · 2026Article
- Mechanochemical feedback between confinement and actin crosslinking drives the shape dynamics of liquid-like droplets.Nature communications · 2026Article
- Characteristic frequencies of localized stress relaxation in scaling-law rheology of living cells.Biophysical journal · 2025Article
- Actin crosslinking by α-actinin averts viscous dissipation of myosin force transmission in stress fibers.iScience · 2023Article
- Simulations of dynamically cross-linked actin networks: Morphology, rheology, and hydrodynamic interactions.PLoS computational biology · 2021Article
- Dynamic actin cross-linking governs the cytoplasm's transition to fluid-like behavior.Molecular biology of the cell · 2020Article
- Phosphorylation of ACTN4 Leads to Podocyte Vulnerability and Proteinuric Glomerulosclerosis.Journal of the American Society of Nephrology : JASN · 2020Article
- Tuning corneal epithelial cell adhesive strength with varying crosslinker content in silicone hydrogel materials.Translational vision science & technology · 2020Article
- Physics and Biology (of Chromosomes).Journal of molecular biology · 2020Article
- Steric regulation of tandem calponin homology domain actin-binding affinity.Molecular biology of the cell · 2019Article
- Disease-causing mutation in α-actinin-4 promotes podocyte detachment through maladaptation to periodic stretch.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Transactivated Epidermal Growth Factor Receptor Recruitment of α-actinin-4 From F-actin Contributes to Invasion of Brain Microvascular Endothelial Cells by MeningiticFrontiers in cellular and infection microbiology · 2018Article
- Filament turnover tunes both force generation and dissipation to control long-range flows in a model actomyosin cortex.PLoS computational biology · 2017Article
- Biomimetic Stress Sensitive Hydrogel Controlled by DNA Nanoswitches.Biomacromolecules · 2017Article
- Actin and Actin-Binding Proteins.Cold Spring Harbor perspectives in biology · 2016Review
- Synaptopodin couples epithelial contractility to α-actinin-4-dependent junction maturation.The Journal of cell biology · 2015Article
- Alpha-actinin binding kinetics modulate cellular dynamics and force generation.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- The role of alpha-actinin-4 in human kidney disease.Cell & bioscience · 2015Article
- Microrheology of highly crosslinked microtubule networks is dominated by force-induced crosslinker unbinding.Soft matter · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Filamentous actin and associated actin binding proteins play an essential role in governing the mechanical properties of eukaryotic cells. They can also play a critical role in disease; for example, mutations in α-actinin-4 (Actn4), a dynamic actin cross-linking protein, cause proteinuric disease in humans and mice. Amino acid substitutions strongly affect the binding affinity and protein structure of Actn4. To study the physical impact of such substitutions on the underlying cytoskeletal network, we examine the bulk mechanical behavior of in vitro actin networks cross-linked with wild-type and mutant Actn4. These networks exhibit a complex viscoelastic response and are characterized by fluid-like behavior at the longest timescales, a feature that can be quantitatively accounted for through a model governed by dynamic cross-linking. The elastic behavior of the network is highly nonlinear, becoming much stiffer with applied stress. This nonlinear elastic response is also highly sensitive to the mutations of Actn4. In particular, we observe that actin networks cross-linked with Actn4 bearing the disease-causing K255E mutation are more brittle, with a lower breaking stress in comparison to networks cross-linked with wild-type Actn4. Furthermore, a mutation that ablates the first actin binding site (ABS1) in Actn4 abrogates the network's ability to stress-stiffen is standard nomenclature. These changes in the mechanical properties of actin networks cross-linked with mutant Actn4 may represent physical determinants of the underlying disease mechanism in inherited focal segmental glomerulosclerosis.
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