597 papers
This study reveals that neurodegeneration risk variants in *TMEM106B* and *GRN* converge to promote the accumulation of intra-lysosomal TMEM106B fibrils, which drive age-related cognitive decline and neuronal damage through impaired degradation and lysosomal rupture.
This study demonstrates that hyperosmolar stress induces corneal epithelial cells to release small extracellular vesicles enriched with metabolic proteins, suggesting these vesicles serve as early biomarkers for dry eye disease by reflecting underlying metabolic changes.
This study reveals that the FOXO3-regulated lncRNA MIR503HG maintains cellular quiescence in human diploid fibroblasts by acting as a competing endogenous RNA (ceRNA) to sequester miR-508, thereby stabilizing PTEN levels and suppressing the PI3K/Akt pathway.
This paper demonstrates that spatial heterogeneities in minimal stochastic reaction-diffusion models are sufficient to fundamentally reshape cell polarization dynamics, explaining phenomena like pole-to-pole oscillations and the New-End Take-Off through mechanisms of stochastic competition and finite cytoplasmic diffusion without requiring complex biochemical motifs.
This study identifies a phosphorylation-regulated "kinesin-kinase code" mediated by NEK10 and the KLC2 CTD that functions as a coincidence detector to control kinesin-1 activation and lysosome transport by integrating adaptor binding with membrane cues.
This study demonstrates that in larval zebrafish, pharmacological vasodilation significantly reduces intracerebral haematoma size by confining red blood cells to affected vessels, whereas vasoconstriction does not exacerbate haemorrhage, thereby establishing vascular dilation as a key modulator of haemorrhage progression.
This study reveals that dynamic UFMylation governs cellular fitness by clearing stalled ER ribosomes to maintain GPT2 levels and endogenous alanine synthesis, thereby orchestrating a multi-organelle proteostasis network essential for survival under specific nutrient conditions.
This study reveals that inhibiting V-ATPase triggers GCN1/GCN2-mediated integrated stress response and rapid MCL-1 depletion, leading to BAX/BAK-dependent apoptosis and creating a therapeutic vulnerability that synergizes with BH3 mimetics in MCL-1-dependent cancers.
This study introduces a novel methodology called fluorophore-mediated optofixation (FLUMO), which utilizes visible light-activated DNA-targeting fluorophores like palmatine to rapidly and precisely fix live cells via reactive oxygen species and lipid peroxidation, enabling high-resolution functional ablation and labeling across single cells, organoids, and whole organisms.
By combining micropatterning with high-throughput spatial mapping, this study establishes that endothelial caveolae exhibit distinct, state-dependent spatial organizations—such as rear localization in migrating cells, peri-junctional clustering in monolayers, and front enrichment in angiogenic vessels—which collectively serve as predictive indicators of vascular stability and remodeling.
This study reveals that nuclear STING exacerbates replication stress and genome instability in progeria and tumor cells by recruiting SAMHD1 to deplete dNTPs and promote MRE11-mediated nascent DNA degradation, thereby establishing a pathological feedforward loop between innate immune signaling and impaired DNA replication.
This study identifies pulmonary venous endothelial cells and the molecule PLVAP as common therapeutic targets across idiopathic pulmonary fibrosis and non-IPF progressive fibrotic interstitial lung diseases, demonstrating that PLVAP knockdown mitigates fibrosis by reducing mesenchymal macrophage interactions.
This study demonstrates that specific mutations in Chlamydomonas γ-tubulin exert dominant-negative effects that compromise the stability of A- and C-tubules within centriolar triplets, leading to protofilament loss and defects in ciliary assembly and nuclear organization despite the retention of the overall nine-triplet structure.
This study reveals that axonal development relies on a novel Golgi-independent pathway where the axonal endoplasmic reticulum couples local transmembrane protein translation and secretion through a feedback loop involving HDLBP and the NRZ-SEC22B tethering complex to facilitate protein delivery to the axonal plasma membrane.
This study reveals that high microtubule occupancy at kinetochores is essential for timely and localized SAC silencing, thereby preventing prolonged mitosis from triggering a p53-dependent "mitotic stopwatch" that blocks daughter cell proliferation.
This study reveals that the DNA damage response kinase ATM not only utilizes the Golgi membrane as a docking platform but also actively restricts Golgi extension and maintains its morphology through GOLPH3 antagonism and substrate phosphorylation, thereby influencing Golgi cargo biology and highlighting a critical crosstalk between the Golgi and the nucleus.
This study leverages AlphaFold 3 to construct a comprehensive, deep-learning-based atlas of the human XPO1-mediated nuclear exportome, identifying over 3,000 high-confidence NESs—including noncanonical patterns and regulatory mechanisms—that significantly expand our understanding of nuclear transport and its dysregulation in disease.
This study utilizes patient-derived human cardiac organoids to demonstrate that LMNA haploinsufficiency triggers early, reversible multicellular remodeling and profibrotic signaling prior to the onset of overt dilated cardiomyopathy, highlighting a potential window for therapeutic intervention.
During intestinal regeneration, polyploid cells efficiently cluster supernumerary centrosomes to form bipolar spindles yet still undergo rapid clearance through mitotic errors and subsequent lineage loss, a conserved mechanism essential for successful tissue maturation.
This study reveals that the yeast transcription factor Cbf1 stabilizes the budding yeast kinetochore by forming an interdependent, mutually reinforcing interaction with the inner kinetochore protein Okp1, which is essential for both CCAN assembly and the protein's own stable centromeric association.