Biology subjects

Shenoy, V.

Publications and source records attributed to Shenoy, V..

At least 19 recordsLinked to original sources

bioRxiv2026

Osmotic Coupling of Mechanics and Epigenetics Regulates Chromatin Phase Organization

Cells experience epigenetic, osmotic, and mechanical perturbations that reorganize chromatin, yet how these distinct cues are integrated into a common physical response of the nucleus remains unclear. Here, we identify nuclear hydration as a central state variable that links microenvironmental perturbations to chromatin phase organization and nuclear mechanics. We develop a non-equilibrium mesoscale model that couples chromatin elasticity, water transport, and epigenetic reaction-diffusion kinetics. In this framework, chromatin behaves as a deformable polymer that segregates into coexisting water-rich euchromatic and water-poor heterochromatic phases, whose compositions and morphologies are regulated by hydration-dependent swelling, elastic strain, and histone-mark interconversion. The model predicts that epigenetic perturbations, osmotic shocks, and volume-changing mechanical loads reorganize chromatin by shifting intranuclear water content, nuclear volume, and euchromatin-heterochromatin phase balance. It further predicts that anisotropic forces impose directional strain, driving heterochromatin elongation, alignment, and lamellar transitions. Quantitative comparisons with super-resolution imaging, AFM and chromatin-accessibility measurement - across pharmacological, osmotic, and mechanical perturbations including confinement and micropatterning - support these predictions. Together, our results establish a chemo-mechano-osmotic framework in which nuclear hydration integrates biochemical and biophysical cues to regulate chromatin organization across scales.

biophysics↗

bioRxiv2026

Recursive feedback between Piezo1 conformation and membrane mechanics drives self-organization into finite clusters

Piezo1 is a major mechanosensitive ion channel through which cells convert physical force into calcium-dependent signaling programs. In living membranes, this conversion depends not only on channel activation, but also on whether Piezo1 channels remain dispersed, assemble into finite clusters, or concentrate at sites where receptor signaling and mechanical forces reorganize the membrane. How single-channel force sensing is amplified into these collective spatial states remains unknown. Here we identify a membrane-feedback mechanism that converts single-channel mechanosensing into self-organized Piezo1 clusters. Coupling channel shape to membrane-cortex elasticity reveals that neighboring channels relax shared deformation fields, generating an effective interaction with short-range attraction opposed by longer-range repulsion. As channel density or membrane tension increases, this balanced interaction shifts Piezo1 from dispersed channels into mesoscale finite clusters. Brownian-dynamics simulations reproduce experimentally observed Piezo1 cluster geometries and swelling-induced cluster growth, while comparisons across distinct cellular systems place Piezo1 organization within a common density-tension framework. Applying the same mechanism to LPS-activated macrophages shows how receptor-induced membrane reorganization locally concentrates Piezo1 above the clustering threshold. Overall, these results recast Piezo1 mechanotransduction from isolated-channel force sensing to a membrane-driven self-organization process that spatially biases force-dependent calcium signaling within cells.

biophysics↗

bioRxiv2026

IntravChip: a vascularized and perfused microfluidic model of the primary tumor microenvironment to collect intravasated tumor cells

Hematogenous metastasis is initiated when tumor cells (TCs) intravasate into the vasculature, yet intravasation remains poorly understood because it is difficult to observe in vivo and intravasated TCs are challenging to isolate. To address these challenges, we developed IntravChip, a continuously perfused microfluidic platform containing a vascularized primary tumor microenvironment (TME) enabling the observation of TC intravasation, and a downstream chamber to collect intravasated TCs. The IntravChip can support a high TC concentration in the TME while maintaining complete vascular perfusion, which we found was necessary to collect intravasated cells. Using MDA-MB-231 breast TCs, we identified an optimal initial TC seeding density that, by day 9, yields a densely populated TME and 100-440 collected intravasated TCs. We validated the IntravChip across several TC types, showing that MDA-MB-231 and MV3 TCs have the highest intravasation rates while MCF-7 TCs have low intravasation efficiency. We also show that the IntravChip is compatible with super-resolution nano-imaging. Our devices enabled high-quality STORM imaging, which revealed that H3K9me3 nanodomains are significantly differentially distributed in intravasated MDA-MB-231 tumor cells compared to those residing in the TME. Finally, the IntravChip was validated as a platform to test the effects of anti-cancer drugs on tumor cells and on the vasculature. We showed that a 5 M concentration of sorafenib reduced intravasation events by 69% without impacting the morphology of the microvascular networks (MVNs), while a 10 M concentration led to a significant decrease in vessel diameter. This platform enables quantitative analysis of TC intravasation, collection of intravasated TCs for characterization, and screening of anti-metastatic therapies.

bioengineering↗

bioRxiv2026

Metabolic starvation-induced cell swelling drives solid stress in tumors

Solid stress shapes tumor growth, invasion, and therapeutic response, yet its physical origin and clinical relevance remain unclear. Here, we develop a mechano-electro-osmotic model integrating metabolic gradients, ion transport, and cellular mechanics to explain residual solid stress emergence in tumor spheroids, common models of solid tumors. We show that solid stress arises predominantly from osmotic cell swelling driven by metabolic deprivation and ion accumulation, rather than proliferation. This mechanism generates a characteristic stress architecture: isotropic compression in the hypoxic core balanced by peripheral tangential tension, causing pronounced cell and nuclear deformation. The resulting nuclear strain provides a mechanical basis for DNA damage and genomic instability implicated in disease progression and treatment resistance. We validate these predictions in breast cancer using MDA-MB-231 spheroids and patient-derived ductal carcinoma in situ lesions, and corroborate them across published spheroid models and in vivo and ex vivo tumors spanning additional cancer types. Our findings link tumor metabolism to clinically relevant mechanical stresses, suggesting opportunities to target osmotic and metabolic pathways to mitigate solid stress and improve therapeutic outcomes.

bioengineering↗

bioRxiv2025

O-SNAP: A comprehensive pipeline for spatial profiling of chromatin architecture

We present O-SNAP (Objective Single-Molecule Nuclear Architecture Profiler), a comprehensive pipeline for the automated extraction, comparison, and classification of nuclear features from single-molecule localization microscopy (SMLM) data. O-SNAP quantifies 144 interpretable, biologically grounded spatial features describing chromatin organization or histone mark distributions at nanoscale resolution. The pipeline includes modules for pairwise comparison of features using volcano plots, feature set enrichment analysis, robust feature selection and classification of cell states, and pseudotime trajectory inference. We validate O-SNAP across diverse biological contexts, including fibroblast-to-stem cell reprogramming, tendon disease, histone variant sensitivity to oxidative stress, and chondrocyte de-differentiation, demonstrating its ability to detect subtle changes in nanoscale chromatin organization across diverse biological transitions.

biophysics↗

bioRxiv2025

Remodeling of self-assembled microvascular networks under long term flow

The incorporation of a functional perfusable microvascular network (MVN) is a common requirement for most organ on-chip-models. Long-term perfusion of MVNs is often required for the maturation of organ phenotypes and disease pathologies and to model the transport of cells and drugs entering organs. In our microphysiological system, we observe that flow can recover perfusion in regressed MVNs and maintain perfusable MVNs for at least 51 days. Throughout the 51 days, however, the MVNs are continuously remodeling to align with the direction of bulk flow and only appear to attain morphological homeostasis with the use of maintenance medium without growth factors. We observed that the flow resistance of the MVNs decreases over time, and using a computational model, we show that stable vessels have higher flow rates and velocities compared to regressing vessels. Cytokine analysis suggests that static conditions generate an inflammatory state, and that continuous flow reduces inflammation over an extended period. Finally, through bulk RNA sequencing we identify that both the endothelial and fibroblast cells are actively engaged in vascular and matrix remodeling due to flow and that these effects persist for at least 2 weeks. This MPS can be applied to study hemodynamically driven processes, such as metastatic dissemination or drug distribution, or to model long-term diseases previously not captured by MPS, such as chronic inflammation or aging-associated diseases.

biophysics↗

bioRxiv2025

Glassy Adhesion Dynamics Govern Transitions Between Sub-Diffusive and Super-Diffusive Cell Migration on Viscoelastic Substrates

Cell migration is pivotal in cancer metastasis, where cells navigate the extracellular matrix (ECM) and invade distant tissues. While the ECM is viscoelastic--exhibiting time-dependent stress relaxation--its influence on cell migration remains poorly understood. Here, we employ an integrated experimental and modeling approach to investigate filopodial cancer cell migration on viscoelastic substrates and uncover a striking transition from sub-diffusive to super-diffusive behavior driven by the substrates viscous relaxation timescale. Conventional motor-clutch based migration models fail to capture these anomalous migration modes, as they overlook the complex adhesion dynamics shaped by broad distribution of adhesion lifetimes. To address this, we develop a glassy motor-clutch model that incorporates the rugged energy landscape of adhesion clusters, where multiple metastable states yield long-tailed adhesion timescales. Our model reveals that migration dynamics are governed by the interplay between cellular and substrate timescales: slow-relaxing substrates prolong trapping, leading to sub-diffusion, while fast-relaxing substrates promote larger steps limiting trapping, leading to super-diffusion. Additionally, we uncover the role of actin polymerization and contractility in modulating adhesion dynamics and driving anomalous migration. These findings establish a mechanistic framework linking substrate viscoelasticity to cell motility, with implications for metastasis and cancer progression.

biophysics↗

bioRxiv2024

Polymer Model Integrates Super-Resolution Imaging and Epigenomic Sequencing to Elucidate the Role of Epigenetic Reactions in Shaping 4D Chromatin Organization

Chromatin, with its complex spatial and temporal organization, plays a crucial role in regulating gene expression. Recent advancements in super-resolution microscopy have revealed that nanoscale domains of heterochromatin (repressed segments) embedded within a euchromatin (active segments) background are fundamental units of 3D chromatin organization. In tissue-resident cells, the size of these heterochromatin domains varies with the microenvironment, particularly its stiffness, and chromatin organization is also influenced by pharmacological and epigenetic drugs. However, the mechanisms governing heterochromatin domain size under various conditions and their impact on gene expression remain unclear. To address this knowledge gap, we have developed a dynamic, next-generation sequencing informed chromatin copolymer model. Our model simulates the spatiotemporal evolution of chromatin, driven by passive diffusion and active epigenetic reactions, which interconvert euchromatin and heterochromatin. By integrating chromatin-chromatin interaction energetics and diffusion-reaction dynamics, we predict the formation of nanoscale heterochromatin-rich domains and establish a scaling relationship between their size and the modulation of epigenetic reaction rates. Additionally, our model predicts that epigenetic and chromatin compaction changes in response to changes in global reaction rates occur predominantly at domain boundaries. We validated these predictions via Hi-C contact map analysis and super-resolution imaging of hyperacetylated melanoma cells. Subsequent RNA-seq analysis suggested a pivotal role of these epigenetic shifts in influencing the metastatic potential of these cells. We further validated our mesoscale findings against chromatin rearrangement in hMSCs, which exhibit sensitivity of epigenetic reaction rates to changes in microenvironmental stiffness. Finally, we evaluated the effects of cycling of epigenetic reaction rates in silico, mimicking the cellular transition to different extracellular conditions, and back again. This finding reveals a cell-type invariant mechanism driven by domain boundaries, whereby chromatin organization guides epigenetic memory formation. Our findings show that chromatin reorganization in response to changes in epigenetic reaction rates resulting from alterations in the microenvironment, drug exposure and disease progression impacts both immediate cellular responses and long-term epigenetic memory.

biophysics↗

bioRxiv2024

Microtubule forces drive nuclear damage in LMNA cardiomyopathy

Nuclear homeostasis requires a balance of forces between the cytoskeleton and nucleus. Mutations in the LMNA gene, which encodes the nuclear envelope proteins lamin A/C, disrupt this balance by weakening the nuclear lamina. This results in nuclear damage in contractile tissues and ultimately muscle disease. Intriguingly, disrupting the LINC complex that connects the cytoskeleton to the nucleus has emerged as a promising strategy to ameliorate LMNA-associated cardiomyopathy. Yet how LINC complex disruption protects the cardiomyocyte nucleus remains unclear. To address this question, we developed an assay to quantify the coupling of cardiomyocyte contraction to nuclear deformation and interrogated its dependence on the nuclear lamina and LINC complex. We found that, surprisingly, the LINC complex was mostly dispensable for transferring contractile strain to the nucleus, and that increased nuclear strain in lamin A/C-deficient cardiomyocytes was not rescued by LINC complex disruption. Instead, LINC complex disruption eliminated the cage of microtubules encircling the nucleus. Disrupting microtubules was sufficient to prevent nuclear damage and rescue cardiac function induced by lamin A/C deficiency. We computationally simulated the stress fields surrounding cardiomyocyte nuclei and show how microtubule forces generate local vulnerabilities that damage lamin A/C-deficient nuclei. Our work pinpoints localized, microtubule-dependent force transmission to the nucleus as a pathological driver and therapeutic target for LMNA- cardiomyopathy. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=131 SRC="FIGDIR/small/579774v5_ufig1.gif" ALT="Figure 1"> View larger version (52K): org.highwire.dtl.DTLVardef@1443daeorg.highwire.dtl.DTLVardef@12d7a8borg.highwire.dtl.DTLVardef@c85900org.highwire.dtl.DTLVardef@14b3c89_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

bioRxiv2023

Fibrillar adhesion dynamics govern the timescales of nuclear mechano-response via the vimentin cytoskeleton

The cell nucleus is continuously exposed to external signals, of both chemical and mechanical nature. To ensure proper cellular response, cells need to regulate not only the transmission of these signals, but also their timing and duration. Such timescale regulation is well described for fluctuating chemical signals, but if and how it applies to mechanical signals reaching the nucleus is still unknown. Here we demonstrate that the formation of fibrillar adhesions locks the nucleus in a mechanically deformed conformation, setting the mechanical response timescale to that of fibrillar adhesion remodelling ([~]1 hour). This process encompasses both mechanical deformation and associated mechanotransduction (such as via YAP), in response to both increased and decreased mechanical stimulation. The underlying mechanism is the anchoring of the vimentin cytoskeleton to fibrillar adhesions and the extracellular matrix through plectin 1f, which maintains nuclear deformation. Our results reveal a mechanism to regulate the timescale of mechanical adaptation, effectively setting a low pass filter to mechanotransduction.

biophysics↗

bioRxiv2023

Microinterfaces in bicontinuous hydrogelsguide rapid 3D cell migration

Cell migration is critical for tissue development and regeneration but requires extracellular environments that are conducive to motion. Cells may actively generate migratory routes in vivo by degrading or remodeling their environments or may instead utilize existing ECM microstructures or microtracks as innate pathways for migration. While hydrogels in general are valuable tools for probing the extracellular regulators of 3D migration, few have recapitulated these natural migration paths. Here, we developed a biopolymer-based (i.e., gelatin and hyaluronic acid) bicontinuous hydrogel system formed through controlled solution immiscibility whose continuous subdomains and high micro-interfacial surface area enabled rapid 3D migration, particularly when compared to homogeneous hydrogels. Migratory behavior was mesenchymal in nature and regulated by biochemical and biophysical signals from the hydrogel, which was shown across various cell types and physiologically relevant contexts (e.g., cell spheroids, ex vivo tissues, in vivo tissues). Our findings introduce a new design that leverages important local interfaces to guide rapid cell migration.

bioengineering↗

bioRxiv2023

Active Transcription and Epigenetic Reactions Synergistically RegulateMeso-Scale Genomic Organization

In interphase nuclei, chromatin is organized into interspersed dense domains with characteristic sizes, both in the nuclear interior and periphery. However, the quantitative impact of transcription and histone modifications on the size and distribution of these domains remains unclear. Here, we introduce a mesoscale theoretical model that investigates the relationship between heterochromatic domain sizes and loop extrusion rates from these domains. The model considers chromatin-chromatin and chromatin-lamina interactions, methylation and acetylation kinetics, and diffusion of epigenetic marks and nucleoplasm. Our model generates testable predictions that help reveal the biophysics underlying chromatin organization in the presence of transcription-driven loop extrusion. This process is kinetically captured through the conversion of heterochromatin to euchromatin in response to RNAPII activity. We discovered that a balance between diffusive and reactive fluxes governs the steady-state sizes of heterochromatin domains. Using theory and simulations, we predicted that a loss of transcription results in increased chromatin compaction and larger heterochromatin domain sizes. To validate our predictions, we employed complementary super-resolution and nano-imaging techniques on five different cell lines with impaired transcription. We quantitatively assessed how domain sizes scale with loop extrusion rates at the hetero-euchromatin interfaces. Our analysis of previously obtained super-resolution images of nuclei revealed that excessive loop extrusion leads to smaller heterochromatin domains. The model successfully recapitulated these observations, explaining how transcription loss can counteract the effects of cohesin overloading. As the general biophysical mechanisms regulating heterochromatin domain sizes are independent of cell type, our findings have significant implications for understanding the role of transcription in global genome organization.

biophysics↗

bioRxiv2023

Actin polymerization drives lumen formation in a human epiblast model

Lumens or fluid-filled cavities are a ubiquitous feature of mammals and are often evolutionarily linked to the origin of body-plan complexity. Post-implantation, the pluripotent epiblast in a human embryo forms a central lumen, paving the way for gastrulation. While osmotic pressure gradients drive lumen formation in many developmental contexts, mechanisms of human epiblast lumenogenesis are unknown. Here, we study lumenogenesis in a pluripotent-stem-cell-based model of the epiblast using engineered hydrogels that model the confinement faced by the epiblast in the blastocyst. Actin polymerization into a dense mesh-like network at the apical surface generates forces to drive early lumen expansion, as leaky junctions prevent osmotic pressure gradients. Theoretical modeling reveals that apical actin polymerization into a stiff network drives lumen opening, but predicts that a switch to pressure driven lumen growth at larger lumen sizes is required to avoid buckling of the cell layer. Consistent with this prediction, once the lumen reaches a radius of around 12 m, tight junctions mature, and osmotic pressure gradients develop to drive further lumen growth. Human epiblasts show a transcriptional signature of actin polymerization during early lumenogenesis. Thus, actin polymerization drives lumen opening in the human epiblast, and may serve as a general mechanism of lumenogenesis.

developmental biology↗

bioRxiv2022

Collective invasion of the basement membrane in breast cancer driven by forces from cell volume expansion and local contractility

Breast cancer becomes invasive when carcinoma cells collectively invade through the basement membrane (BM), a nanoporous layer of matrix that physically separates the primary tumor from the stroma, in a first step towards metastasis. Single cells can invade through nanoporous three-dimensional (3D) matrices via protease-mediated degradation or, when the matrix exhibits sufficient mechanical plasticity, force-mediated widening of pores. However, how cells invade collectively through physiological BM layers in cancer remains unclear. Here, we developed a 3D in vitro model of collective invasion of the BM during breast cancer. We show that cells utilize both proteases and forces to breach the BM. Forces are generated from a combination of global cell volume expansion that stretch the BM with local contractile forces that act in the plane of the BM to breach it, allowing invasion. These results uncover a mechanism by which cells collectively interact to overcome a critical barrier to metastasis.

cancer biology↗

bioRxiv2022

FBXO11 deficiency in mice impairs lung development and aggravates cigarette smoke-induced airway fibrosis

Small airway fibrosis is a common pathology of chronic obstructive pulmonary disease (COPD) and contributes to airflow obstruction. However, the underlying fibrogenic mechanism is poorly understood. Epithelial-mesenchymal transition (EMT) has been proposed as a driver of fibrosis. EMT occurs in the airways of COPD patients and smokers, but it remains elusive whether EMT may contribute to airway fibrosis. We previously reported that FBXO11 is a critical suppressor of EMT and Fbxo11 deficiency in mice causes neonatal lethality and EMT in epidermis. Here, we found that Fbxo11-deficient mouse embryonic lungs showed impaired epithelial differentiation, excess fibroblast cells surrounding the airways, and thickened interstitial mesenchyme. We further generated conditional mutant mice to ablate Fbxo11 selectively in the club airway epithelial cells in adult mice, which induced partial EMT in the airways. To determine the effect of EMT on airway fibrosis, Fbxo11 conditional mutant mice were exposed to cigarette smoke. Airway-specific loss of Fbxo11 markedly enhanced smoking-induced airway fibrotic remodeling and collagen deposition. Taken together, our study suggests that EMT in the airway epithelium exacerbates cigarette smoke-induced airway fibrosis.

cell biology↗

bioRxiv2022

Vimentin Intermediate Filaments Can Enhance or Abate Active Cellular Forces in a Microenvironmental Stiffness-Dependent Manner

The mechanical properties of cells are largely determined by the cytoskeleton, which is a complex network of interconnected biopolymers consisting of actin filaments, microtubules, and intermediate filaments. While disruption of the actin filament and microtubule networks is known to decrease and increase cell-generated forces, respectively, the effect of intermediate filaments on cellular forces is not well understood. Using a combination of theoretical modeling and experiments, we show that disruption of vimentin intermediate filaments can either increase or decrease cell-generated forces, depending on microenvironment stiffness, reconciling seemingly opposite results in the literature. On the one hand, vimentin is involved in the transmission of actomyosin-based tensile forces to the matrix and therefore enhances traction forces. On the other hand, vimentin reinforces microtubules and their stability under compression, thus promoting the role of microtubules in suppressing cellular traction forces. We show that the competition between these two opposing effects of vimentin is regulated by the microenvironment stiffness. For low matrix stiffness, the force-transmitting role of vimentin dominates over their microtubule-reinforcing role and therefore vimentin increases traction forces. At high matrix stiffness, vimentin decreases traction forces as the microtubule-reinforcing role of vimentin becomes more important with increasing matrix stiffness. Our theory reconciles seemingly disparate experimental observations on the role of vimentin in active cellular forces and provides a unified description of stiffness-dependent chemo-mechanical regulation of cell contractility by vimentin. SignificanceVimentin is a marker of the epithelial to mesenchymal transition which takes place during important biological processes including embryogenesis, metastasis, tumorigenesis, fibrosis, and wound healing. While the roles of the actin and microtubule networks in the transmission of cellular forces to the extracellular matrix are known, it is not clear how vimentin intermediate filaments impact cellular forces. Here, we show that vimentin impacts cellular forces in a matrix stiffness-dependent manner. Disruption of vimentin in cells on soft matrices reduces cellular forces, while it increases cellular forces in cells on stiff matrices. Given that cellular forces are central to both physiological and pathological processes, our study has broad implications for understanding the effect of vimentin on cellular forces in different microenvironments.

biophysics↗

bioRxiv2022

Tension anisotropy drives phenotypic transitions of cells via two-way cell-ECM feedback

Mechanical factors such as stress in the extracellular environment are known to affect phenotypic commitment of cells. However, the stress fields experienced by cells in tissues are multiaxial, and the ways that cells integrate this multiaxial information are largely unknown. Here, we report that the anisotropy of these stress fields is a critical factor triggering phenotypic transition in fibroblast cells, outweighing the previously reported role of stress amplitude. Using a combined experimental and computational approach, we discovered a self-reinforcing mechanism in which cellular protrusions interact with collagen fibers to develop tension anisotropy, which in turn stabilizes protrusions and amplifies their contractile forces. Disruption of this self-reinforcing process, either by reducing tension anisotropy or by inhibiting contractile protrusions, prevented phenotypic conversion of fibroblasts to contractile myofibroblasts.

biophysics↗

bioRxiv2021

Chemo-mechanical Diffusion Waves Orchestrate Collective Dynamics of Immune Cell Podosomes

Immune cells, such as macrophages and dendritic cells, can utilize podosomes, actin-rich protrusions, to generate forces, migrate, and patrol for foreign antigens. In these cells, individual podosomes exhibit periodic protrusion and retraction cycles (vertical oscillations) to probe their microenvironment, while multiple podosomes arranged in clusters demonstrate coordinated wave-like spatiotemporal dynamics. However, the mechanisms governing both the individual vertical oscillations and the coordinated oscillation waves in clusters remain unclear. By integrating actin polymerization, myosin contractility, actin diffusion, and mechanosensitive signaling, we develop a chemo-mechanical model for both the oscillatory growth of individual podosomes and wave-like dynamics in clusters. Our model reveals that podosomes show oscillatory growth when the actin polymerization-associated protrusion and the signaling-associated myosin contraction occur at similar rates, while the diffusion of actin monomers within the cluster drives mesoscale coordination of individual podosome oscillations in an apparent wave-like fashion. Our model predicts the influence of different pharmacological treatments targeting myosin activity, actin polymerization, and mechanosensitive pathways, as well as the impact of the microenvironment stiffness on the wavelengths, frequencies, and speeds of the chemo-mechanical waves. Overall, our integrated theoretical and experimental approach reveals how collective wave dynamics arise due to the coupling between chemo-mechanical signaling and actin diffusion, shedding light on the role of podosomes in immune cell mechanosensing within the context of wound healing and cancer immunotherapy.

biophysics↗