Results 131 to 140 of about 181,087 (306)
A post‐stroke perivascular niche of microglia characterized by low expression of M2 markers and elevated glycolysis, oxidative phosphorylation (OXPHOS), and phagocytic activity is identified, which is termed stroke‐activated vascular‐associated microglia (stroke‐VAM).
Yanan Li +8 more
wiley +1 more source
TRIM38 Suppresses Breast Cancer Progression via Modulating SQSTM1 Ubiquitination and Autophagic Flux
TRIM38, an E3 ubiquitin ligase, suppresses breast cancer progression by inhibiting proliferation, migration, and invasion. Downregulated in breast tumor, its loss correlates with poor prognosis. Mechanistically, TRIM38 mediates K63‐linked ubiquitination of SQSTM1/p62 at K420, disrupting SQSTM1‐LC3 interaction and blocking autophagic flux.
Shan Jiang +14 more
wiley +1 more source
Fcgamma receptor-mediated phagocytosis in macrophages lacking the Src family tyrosine kinases Hck, Fgr, and Lyn. [PDF]
Macrophage Fcgamma receptors (FcgammaRs) mediate the uptake and destruction of antibody-coated viruses, bacteria, and parasites. We examined FcgammaR signaling and phagocytic function in bone marrow-derived macrophages from mutant mice lacking the major ...
Crowley, MT +6 more
core
The Gut Microbiota Regulates Motor Deficits via Butyrate in a Gnal+/− Mouse Model of DYT25 Dystonia
The present study provides compelling evidence for a modulatory role of the gut microbiota in the pathology of DYT25 dystonia, and butyrate supplementation alleviates the motor deficits of dystonia in Gnal+/− mice. Abstract Dystonia is the third most common movement disorder, following essential tremor and Parkinson's disease. The underlying mechanisms
Jingya Guo +3 more
wiley +1 more source
B cell reductive therapy with rituximab in the treatment of rheumatoid arthritis. [PDF]
The approach to treating autoimmune disorders is currently undergoing a significant change in focus. As therapies are developed that are more precise in targeting the pathogenesis for these diseases, patients experience significantly fewer side effects ...
Sands, Jacob, Tuscano, Joseph M
core +2 more sources
Phospholipid transfer protein(PLTP) plays a critical role in forming a complex with kinase A (AURKA) and P65. This interaction facilitates phosphorylation of P65 at Ser536, leading to the activation of the NF‐κB signaling pathway. Ultimately, this leads to the upregulation of downstream cytokines, including IL‐6, IL‐8, and CSF‐1, which promotes M2 ...
Xinyue Liang +14 more
wiley +1 more source
Extracellular vesicles (EVs) released from TGF‐β‐activated CAFs are enriched with ECM proteins such as TSG6 and THBS1, which facilitate their binding to recipient cell membranes. This EV–cell interaction promotes the clustering of CD44 and TGF‐β receptors on the target cell surface, thereby potentiating TGF‐β signaling activity. This study highlights a
Chao Li +7 more
wiley +1 more source
Genetically Engineered T-Cells for Malignant Glioma: Overcoming the Barriers to Effective Immunotherapy. [PDF]
Malignant gliomas carry a dismal prognosis. Conventional treatment using chemo- and radiotherapy has limited efficacy with adverse events. Therapy with genetically engineered T-cells, such as chimeric antigen receptor (CAR) T-cells, may represent a ...
Almeida, Neil D +4 more
core
Lei et al. demonstrate that cancer stem cells (CSCs) play a pivotal role in impairing the differentiation of CD103+ T cells in patients with non‐small‐cell lung cancer. The key mechanism involves CSC‐derived acetyl‐CoA, which disrupts CD103+ T cell differentiation by sequentially inducing acetylation and ubiquitination of the Blimp‐1 protein. Targeting
Jiaxin Lei +10 more
wiley +1 more source
Solid predominant lung adenocarcinoma exhibits an immune‐excluded, ferroptosis‐resistant niche enriched with IL4I1⁺ TAMs and TDO2⁺ myCAFs. Spatial and multi‐omics analyses reveal AhR‐driven crosstalk that promotes T cell exhaustion and therapy resistance. Blocking AhR with CH‐223191 restores ferroptosis sensitivity, and its combination with ferroptosis
Zhaoxuan Wang +16 more
wiley +1 more source

