Results 161 to 170 of about 134,903 (295)
Depletion of the RNA‐Editing Enzyme ADAR1 Invigorates the Antitumor Immunity of NK Cells
ADAR1 is upregulated in NK cells from melanoma patients, impairing their function. Its loss enhances NK cell tumor infiltration and cytotoxicity in vitro and in vivo. Mechanistically, ADAR1 deficiency destabilizes CD38 mRNA to reduce its expression, thereby increasing NK cell mobility and killing, which nominates it as a therapeutic target for NK cell ...
Shuhan Chen +11 more
wiley +1 more source
Ng et al. show that the BCR::ABL1 kinase that drives the lymphoid leukemia Ph+B‐ALL modulates enhancer function by coopting signaling‐inducible transcription factors such as MYC, STAT5, and ETV5. BCR::ABL1 thereby promotes the transcriptional program driving and defining this leukemia and renders Ph+B‐ALL cells hypersensitive to enhancer‐inhibiting ...
Han Leng Ng +19 more
wiley +1 more source
Self‐Assembling Hybrid Hydrogel Reprograms the Stromal Vascular Fraction to Treat Osteoarthritis
This study presents a bioinspired injectable hydrogel that enhances the therapeutic potential of stem cell‐rich stromal vascular fraction for treating osteoarthritis. By reprogramming cell behavior through epigenetic modulation, the hydrogel promotes cartilage regeneration and reduces joint damage in a rat model, offering a promising new approach for ...
Waifang Hou +23 more
wiley +1 more source
ABSTRACT Our previous clinical trials had demonstrated that neoadjuvant hypofractionated radiotherapy (HFRT) combined with immunotherapy yields promising clinical outcomes in locally advanced rectal cancer (LARC). However, this combined modality benefits only a subset of patients, highlighting the need to uncover the mechanisms underlying how ...
Lichao Liu +12 more
wiley +1 more source
Lung cancer remains the leading cause of cancer‐related death. We investigated the role of the epigenetic regulator DMAP1 in NSCLC and found that its loss induces replication stress and DNA damage. This in turn activates type I IFN signaling via the cGAS–STING pathway and transcriptional ISG de‐repression, enhancing anti‐tumor immune responses ...
Kan Huang +10 more
wiley +1 more source
Emerging evidence suggests that intraneuronal Aβ accumulation represents an early pathogenic event in Alzheimer's disease (AD). Using Drosophila AD model, this study shows that a nonsecreted serine protease Yip7 physically interacts with Aβ. This causes intraneuronal Aβ accumulation but surprisingly reduces the associated neurotoxicity, arguing that ...
Jingyun Su +4 more
wiley +1 more source
4‐HBA upregulates NKIRAS2 levels, inhibiting the activation of the NF‐κB pathway and subsequently reducing the levels of neuroinflammatory markers. This modulation helps restore normal mood and behavior in hyperlipidemic conditions, providing a potential therapeutic strategy for managing hyperlipidemia‐associated depression.
Ying Zhang +7 more
wiley +1 more source
A Functionally Conserved Enhancer is Critical for PGC1A Expression and Thermogenesis in Brown Fat
An evolutionarily conserved enhancer controls PGC1A expression and thermogenic activation in brown adipose tissue. Integrative multi‐omics analyses identify two BAT‐specific enhancers, with PGC1A‐En1 functioning as the dominant regulatory element that maintains thermogenic capacity across species.
Duo Su +10 more
wiley +1 more source
AUTACE is a bifunctional nanoplatform that integrates tumor targeting, immune engagement, and on‐demand KRAS degradation. It targets KRAS/TP53 co‐mutant tumors via TP53‐specific TCRs, elicits antitumor CD8+ T‐cell responses through surface anti‐CD3 antibodies, and uses low‐intensity focused ultrasound (LIFU) to trigger controlled release of the KRAS ...
Luo Li +6 more
wiley +1 more source
This study identifies GDF15+ TAMs as a cell subset mediating tumor regression after immunotherapy. Macrophage‐intrinsic GDF15 enhances phagocytosis and antigen cross‐presentation to CD8+ T cells through the NF‐κB signaling pathway, thereby inhibiting tumor progression.
Xinyu Zhou +9 more
wiley +1 more source

