556 papers
This study demonstrates that Reelin acts as a novel regulator of endothelial plasticity and vascular remodeling by engaging non-canonical FAK- and AKT-dependent signaling pathways to enhance cell migration and induce a remodeling-permissive phenotype without triggering full endothelial-to-mesenchymal transition.
This study demonstrates that nanovibrational stimulation rapidly induces actin-myosin mediated stiffening and solid-like behavior in NIH 3T3 fibroblasts, though prolonged exposure may eventually reverse these effects, highlighting the importance of temporal optimization for enhancing mechanotransduction.
This study introduces spatial Organellomics (sOrganellomics), an imaging workflow that leverages multi-organelle features to map functional cell state diversity and metabolic adaptation in tissues, revealing novel hepatocyte organization patterns and linking architectural remodeling to bioenergetic heterogeneity in vivo.
This study demonstrates that IntraFlagellar Transport proteins IFT52 and IFT70 directly bind to the mitotic kinesin HSET to induce its oligomerization, thereby enhancing its processivity and ability to organize microtubule networks for efficient centrosome clustering.
This study establishes a novel methodology for identifying, purifying, and characterizing rare mast cells in murine liver fibrosis, revealing their specific expression signatures, low abundance, and significant correlation with disease severity across both mouse models and human transcriptomic data.
Through experimental evolution of *Saccharomyces cerevisiae*, researchers demonstrated that cell size can be reduced four-fold while maintaining homeostasis and fitness, identifying mutations in the Cln3, Sch9, and Rim15 pathways as the primary drivers of this evolutionary plasticity.
This study reveals that alphaherpesviruses (HSV-1 and PRV) hijack the host DNA damage response by inducing the nuclear export and cytosolic MDM2-mediated degradation of class I histone deacetylases (HDAC1/2), a mechanism essential for efficient viral replication and a promising target for therapeutic intervention.
This study demonstrates that AT2-intrinsic expression of misfolded Z-AAT protein drives conserved proteotoxic and inflammatory stress responses, leading to aberrant cell fate adoption and increased susceptibility to emphysema, thereby establishing a cell-autonomous mechanism contributing to Alpha-1 antitrypsin deficiency pathogenesis beyond the traditional protease-antiprotease imbalance.
This study reveals that a Western-style diet promotes colorectal cancer risk by inducing gut dysbiosis, specifically the expansion of *Enterotoxigenic Bacteroides fragilis*, which suppresses canonical Lgr5 stem cells and reprograms c-Kit+ reserve stem cells into a proliferative, tumor-susceptible state via Wnt signaling.
Using a mouse model of 5-fluorouracil-induced mucositis, this study reveals that chemotherapy-induced oral mucosal injury is primarily driven by p53-mediated cell cycle arrest rather than apoptosis, accompanied by unique metabolic reprogramming and diverse epithelial progenitor dynamics that collectively determine tissue repair outcomes.
This study identifies the histone methyltransferase Dot1L as an epigenetic gatekeeper that restricts adult bone regeneration, demonstrating that its genetic or pharmacological inhibition expands injury-responsive CXCL12⁺ stromal progenitors and accelerates early bone formation.
This study demonstrates that a single session of high-frequency (10 Hz) repetitive magnetic stimulation suppresses autophagy and attenuates LPS-induced inflammation and M1 polarization in THP-1-derived macrophages, suggesting its potential as a therapeutic strategy for inflammatory and autophagy-related diseases.
This study demonstrates that chronic local IFNγ signaling from CD8+ T cells in tertiary lymphoid structures actively represses the regenerative capacity of aged alveolar type II cells, a decline that can be partially reversed by neutralizing this inflammatory pathway.
The Universal Cell Embedding (UCE) is a self-supervised foundation model trained on diverse, unannotated single-cell data that creates a unified latent space capable of representing millions of cells across species and tissues, enabling the discovery of new biological insights, developmental lineages, and functional annotations without requiring additional labeling or fine-tuning.
This study reveals that MLL2 facilitates pluripotent cell differentiation by non-catalytically stabilizing 3D chromatin loops associated with bivalent promoters, a structural function essential for lineage commitment that operates independently of its H3K4 trimethyltransferase activity.
This paper presents FARO, a fully automated, real-time feedback control microscopy platform that dynamically adjusts optogenetic stimulation patterns based on live cell behavior to enable reproducible, high-throughput interrogation of spatiotemporal signaling across various biological scales.
This study demonstrates that inhibiting the lipid kinase PIKfyve causes endosomal swelling, which creates a biophysical barrier of increased membrane tension that prevents viral membrane fusion and genome release for specific enveloped viruses, regardless of preserved endosomal acidity.
This paper introduces a counterfactual, ligand-receptor-agnostic framework that quantifies directional cell-cell influence in spatial transcriptomics by measuring state displacements upon neighbor replacement, demonstrating robust, asymmetric interactions in human cholangiocarcinoma through rigorous statistical validation.
This study demonstrates that BNIP3-mediated mitophagy is essential for relieving mitochondrial stress during osteoblast differentiation, and its absence in male mice leads to impaired bone formation and reduced bone mass.
This study reveals that tubulin overexpression disrupts cellular homeostasis by inducing mitotic defects and proteostasis failure through mitochondrial stress and translation attenuation, while nutrient deprivation triggers tubulin downregulation, thereby establishing a critical link between tubulin levels, autoregulation, and cellular quality control.