371 papers
Pirfenidone ameliorates obesity-driven steatohepatitis by differentially remodeling adipose tissue through mTORC1 signaling, specifically inhibiting lipogenesis in subcutaneous fat and suppressing fibrosis in visceral fat to improve liver health.
This study reveals that the nuclear speckle protein SON safeguards the efficient splicing of short, GC-rich introns with weak splice sites by stabilizing core splicing factor recruitment, thereby enabling the high expression of evolutionarily expanded essential genes.
This study reveals that ATM safeguards DNA replication by preventing aberrant PRIMPOL-dependent repriming at spontaneous oxidative base lesions, and its absence creates replication gaps that require homologous recombination for repair, thereby driving synthetic lethality with PARP inhibitors.
FreeTrace is a novel single-molecule tracking framework that utilizes fractional Brownian motion and deep learning to overcome the limitations of traditional Brownian motion assumptions, enabling robust and accurate analysis of anomalous diffusion even in short, crowded intracellular trajectories.
This study reveals that free-roaming dogs and diverse rodent species in rural Tha Wang Pha, Thailand, serve as reservoirs for multiple pathogenic *Leptospira* species, including the first confirmed detection of *L. weilii* in Thai rodents, highlighting a complex transmission cycle that bridges animal habitats and human settlements and underscores the need for integrated One Health surveillance.
This study demonstrates that while native codon sequences are generally sufficient for robust mammalian glycoprotein expression, a skewed codon strategy utilizing the most abundant codons can occasionally enhance yields, all evaluated using a newly developed open-source Golden Gate compatible vector called pTipi.
This study reveals that PARG inhibition triggers the sequestration of essential PAR-binding DNA repair proteins, such as XRCC1, into non-functional nuclear condensates, thereby depleting the repair pool and causing synthetic lethality in cells lacking these factors, a mechanism distinct from PARP inhibitor toxicity which relies on homologous recombination deficiency.
This study demonstrates that the G126S mutation in the cytochrome b gene alone is sufficient to confer high-level bifenazate resistance in a Russian *Tetranychus urticae* population, as evidenced by its rapid fixation to 90% frequency under laboratory selection and its structural impact on the target protein.
This study characterizes a rare case of undetected HIV superinfection in an HLA-B*57:03-positive individual, demonstrating how a pre-adapted superinfecting strain undermines immune control and drives sequential reservoir reactivation and immune-driven viral rebound dynamics during treatment interruption.
This systematic review and meta-analysis of human FRDA transcriptomic data reveals cell type-specific transcriptional dysregulation underlying selective vulnerability, identifies candidate biomarkers such as MYH14, MEG9, and MEG8, and demonstrates their pharmacological modifiability through an interactive community resource.
This study expands the known interactome of the transcriptional co-regulator HCF1 by identifying diverse canonical and non-canonical binding partners, elucidating how extended molecular determinants and register-shifted sequences govern affinity-dependent transcriptional activity and O-GlcNAcylation.
This study utilizes single-cell RNA sequencing to characterize the cellular heterogeneity of the ISE6 tick cell line and reveals that Ehrlichia muris eauclairensis infection induces time-dependent transcriptional shifts, initially upregulating stress and metabolic pathways before downregulating cell cycle and cytoskeletal genes, thereby confirming the cell line's utility for studying tick-pathogen interactions.
This study reveals that the FGBP-binding inhibitor ZW-1261 disrupts HIV-1 capsid integrity by converting essential pentameric subunits into hexamer-like conformations, thereby preventing the formation of closed conical cores.
This study identifies 5,945 tissue-conserved m6A sites across 24 human tissues that are mediated by RBM15/B and linked to mRNA decay, revealing a stable epitranscriptomic layer regulating essential genes whose disruption is associated with transcriptional dysregulation in cancer.
This study demonstrates that treating a Down syndrome mouse model with the HDAC inhibitor SAHA restores histone acetylation, normalizes the transcriptome and chromatin accessibility, and rescues memory deficits by inducing unexpected heterochromatization of the supernumerary chromosome.
This study utilizes cryo-EM to reveal the structural dynamics of transcription-translation coupling in *E. coli*, demonstrating how the flexibility of NusG and NusA accommodates ribosome conformational changes during translation and how steric clashes in collided complexes inhibit ribosome movement and trigger transcription termination.
Despite previous reports linking TTC22 to colon adenocarcinoma metastasis in humans, this study demonstrates that CRISPR-Cas9-mediated inactivation of the Ttc22 gene in C57BL/6N mice results in no observable phenotypic abnormalities, including normal development, fertility, and tumor incidence.
This study reveals that KMT2D deficiency accelerates chondrocyte hypertrophy and senescence in Kabuki syndrome type 1 by increasing mitochondrial ROS production, a process that can be mitigated by ROS neutralization or hypoxia to restore normal bone growth.
This study demonstrates that a lipid nanoparticle-delivered circRNA encoding an engineered human-like uricase effectively and safely lowers serum urate levels for extended periods in a mouse model of hyperuricemia, offering a promising long-term therapeutic strategy for the condition.
This study demonstrates that intensive fishing pressure induces distinct DNA methylation patterns in the marine fish *Xyrichtys novacula* even in genetically homogeneous populations, suggesting that epigenetic mechanisms may facilitate rapid adaptation to anthropogenic selection independently of genetic evolution or age-truncation effects.