Results 181 to 190 of about 62,378 (298)
SeNSs provide a biocompatible, anti‐inflammatory UC therapy. SeNSs form protein coronas enriched with AKT/PI3K/NF‐κB pathway proteins, suppress GP130 via hydrophobic interactions, and inhibit pro‐inflammatory cytokines. In DSS‐induced UC mice, SeNSs reduce inflammation, tissue damage, and disease activity by modulating cytokine, chemokine, and ...
Dingyi Shen+5 more
wiley +1 more source
This study reveals that the glycolytic enzyme HK2 mediates hypoxia‐induced astrocytic exosome biogenesis by directly phosphorylating nSMase1. These astrocytic exosomes impair brain endothelial tight junctions. Astrocyte‐specific knockdown of HK2 reduces exosome release and alleviates brain injury after MCAO.
Chen Chen+12 more
wiley +1 more source
The human exosome: an autoantigenic complex of exoribonucleases in myositis and scleroderma [PDF]
Rick Brouwer+2 more
openalex +1 more source
Brain metastases (BM) from lung cancer are aggressive with poor prognosis. This review covers clinical features, diagnosis, early metastasis, and multi‐omics‐elucidated mechanisms, especially the tumor microenvironment of lung cancer with BM. It also discusses preclinical models, signaling pathways, and emerging therapies.
Yixiang Zhu+5 more
wiley +1 more source
Poly(A) Tail-dependent Exonuclease AtRrp41p fromArabidopsis thaliana Rescues 5.8 S rRNA Processing and mRNA Decay Defects of the Yeast ski6 Mutant and Is Found in an Exosome-sized Complex in Plant and Yeast Cells [PDF]
Julia A. Chekanova+3 more
openalex +1 more source
Cisplatin causes reactive oxygen species accumulation, leading to apoptosis and inflammation in cochlear hair cells. Small extracellular vesicles primarily derived from the damaged hair cells likely contribute to cisplatin‐induced ototoxicity, carrying a variety of microRNAs and proteins.
Jingru Ai+14 more
wiley +1 more source
Ski7p G protein interacts with the exosome and the Ski complex for 3'-to-5' mRNA decay in yeast [PDF]
Yasuhiro Araki
openalex +1 more source
KRAS mutations dynamically remodel the tumor microenvironment (TME), fostering immunosuppression, metabolic symbiosis, and stromal plasticity. This review dissects how oncogenic KRAS variants sculpt TME networks and explores actionable vulnerabilities. Emerging strategies combining KRAS inhibitors and TME‐editing approaches offer potential to dismantle
Jiayao Ma+9 more
wiley +1 more source