597 papers
This study demonstrates that human mitochondrial DNA variants influence telomere length by modulating mitochondrial metabolism and reactive oxygen species production, where reduced Complex I activity leads to telomere shortening via NAD depletion and oxidative stress, a process reversible by antioxidant or NAD precursor supplementation.
This study reveals that DNA damage triggers the conserved phosphorylation of Hsp70 at threonine 495, which locks the chaperone in an open conformation to regulate G1/S cell cycle progression and delay division until repair is complete.
This study presents a human embryonic stem cell toolkit lacking 23 lysosomal storage disorder genes, coupled with multi-omics analyses and cryo-electron tomography, to define distinct proteomic signatures, mitochondrial vulnerabilities, and synaptic defects in cortical and dopaminergic neurons.
This study identifies ATF4 as a master regulator of stress-induced mitochondrial plasticity, demonstrating that it drives the formation of elongated "mega-mitochondria" and nanotunnels by directly activating an NRF1/Nrf2-MFN2 signaling axis to enhance cellular aerobic capacity.
This study reveals that single-cell variability in hormone response magnitude within mammary organoids and human ERα+ cancer cells is driven not by receptor abundance alone, but by the balance of transcriptional co-regulators and distinct activation kinetics.
The study demonstrates that CAP-1902, a novel MasR agonist, acts as a mitophagy inducer that enhances mitochondrial turnover by activating the AMPK/ULK1/FUNDC1 pathway and stimulating biogenesis, thereby rescuing bioenergetic defects and reducing the integrated stress response in human fibroblasts with Complex III deficiency.
The study identifies a self-sustaining FGF7-FGFR2-KLF4 feedback loop in epithelial cells that suppresses pro-inflammatory gene expression, offering a potential therapeutic strategy for treating inflammatory skin and epithelial diseases.
This study demonstrates that nucleus-scale concave microcavities, which mimic the bone microenvironment, induce adaptive nuclear rounding, chromatin compaction, and selective YAP/TAZ-mediated mechanotransduction in human osteosarcoma cells without triggering inflammatory or apoptotic pathways.
This study reveals that cold-induced remodeling of endoplasmic reticulum-plasma membrane contacts and subsequent STIM-mediated calcium influx are essential for maintaining brown adipocyte health, mitochondrial function, and whole-body metabolic homeostasis during thermogenesis.
This study demonstrates that PARKIN is a dual-compartment regulator essential for skeletal muscle regeneration, where it coordinates mitochondrial quality control in quiescent stem cells and nuclear RNA processing upon activation to ensure balanced lineage progression and tissue repair.
By integrating in vitro experiments with computational modeling, this study reveals that soluble factors from DENV-infected cells trigger a temporally distinct sequence of inflammatory and reparatory responses in endothelial cells, ultimately driving dysfunction through the upregulation of SNA1, CDH2, IL6, and FN1.
This study demonstrates that DOT1L-mediated H3K79me3 enrichment at the *RELA* promoter, facilitated by AF10 and AF9, drives NF-κB p65-dependent inflammatory activation in endothelial cells, identifying this epigenetic mechanism as a potential therapeutic target for atherosclerosis.
This study utilizes an optimized MemPrep workflow to define the mammalian ER lipidome, revealing that despite the functional segregation of sheet and tubule proteins, these subdomains share a nearly identical lipid environment dominated by phosphatidylcholine and mono-unsaturated glycerophospholipids that co-evolved with ER-resident proteins to meet shared biophysical constraints.
This study reveals that background-specific mutations in the widely used S288C yeast strain, particularly in the *MKT1* gene, cause pathological mitochondrial dysfunction that mimics an aging pathway, thereby distorting apparent aging trajectories and obscuring genuine age-associated phenotypes.
This study demonstrates that the Arp2/3 complex in postnatal myofibers actively drives muscle growth by generating membrane protrusions that facilitate the fusion of satellite cell-derived myoblasts, thereby establishing myofibers as autonomous regulators of their own nuclear accretion.
This study reveals that Transcription Termination Factor 2 (TTF2) acts as a conserved regulator that ensures proper transcriptional shutdown and prevents premature RNA Polymerase I reactivation during mitotic exit, thereby coordinating the timely resumption of rRNA synthesis and maintaining nucleolar integrity.
This study reveals that in ATM-deficient cells, the BRCA1-A complex restricts replication fork reversal to suppress end-resection and enforce hypersensitivity to Topoisomerase I inhibitors, whereas loss of BRCA1-A restores fork reversal and resection, thereby conferring drug resistance.
This study reveals that miR-378a and NPNT coordinately regulate podocyte autophagy through distinct mechanisms, with miR-378a enhancing flux via mTOR inhibition and NPNT modulating it through MAPK-dependent signaling, offering new insights into the molecular drivers of glomerular diseases.
This study reveals that nascent transcripts from a specific LL2R tandem repeat array on chicken chromosome 2 act as architectural RNAs that nucleate locus-specific, membraneless RNP condensates by recruiting splicing factors while excluding specific hnRNPs, thereby providing a mechanistic model for the formation of nuclear speckles and stress bodies.
This study identifies N-acylphosphatidylethanolamines (NAPEs) as endogenous regulators that inhibit LRRK2 kinase activity to restore lysosomal homeostasis and clear alpha-synuclein aggregates, revealing a promising metabolic axis for Parkinson's disease therapeutics.