BTN3A2 (Butyrophilin Subfamily 3 Member A2)

This pathway promotes melanoma cell proliferation, migration, and resistance to temozolomide...These findings establish RPL18 as a key coordinator of melanoma progression by linking tumor-intrinsic pathways with microenvironmental regulation. Targeting the RPL18-BTF3-STAT3 axis may improve therapeutic responses in melanoma and other cancers with heightened STAT3 activity.

qRT-PCR and Western blot confirmed consistent downregulation (BCL6, PTX3, IL7R) and upregulation (BTN3A2, LGALS1) at both mRNA and protein levels in septic mice compared to controls, supporting MR-based predictions. We identified and experimentally validated 6 sepsis-associated genes and 21 proteins, providing crucial insights into potential therapeutic targets and enhancing understanding of the molecular pathogenesis of sepsis.

TTF1-NP inhibites BTF3, promoting HIF-1α ubiquitination to suppress glycolysis and hepatoma growth, these results offer a novel dual-targeted anti-tumor strategy and lay a solid foundation for the development of S. sorbifolia and TTF1-NP as innovative anti-tumor candidate drugs.

This study establishes epigenome-immune crosstalk in HCC by identifying BTN3A2, S100A12 and TRIM27 as central methylation-immunoregulatory hubs. The discovered methylation-immune axes provide mechanistic insights for developing combination therapies targeting epigenetic checkpoints to reverse immunosuppressive microenvironments in advanced HCC.

Our study uncovers a "plier-like gripping" mechanism, where BTN multimers bridge the TCR surface to drive activation. These findings establish a structural foundation for γδ T cell-targeted immunotherapies distinct from αβ T cell strategies reliant on major-histocompatibility-complex-mediated antigen presentation.

Cryo-EM reveals that BTN2A1-BTN3A1-BTN3A2 binds two γδ TCR ectodomains, with one being sandwiched between the IgV domains of BTN2A1 and BTN3A2, while the other interacts with the free BTN2A1 IgV in the complex, as evidenced by functional data. Together, our findings uncover the mechanism of ligand-induced inside-out stabilization of BTN receptor complexes for dimeric activation of γδ TCR.

Our integrative approach reveals that causal gene expression profiles differ markedly between bulk-tissue and specific brain cell types, emphasizing cellular heterogeneity in MDD pathogenesis and informing precision therapeutic strategies. These findings underscore the necessity of considering cell type-specific gene regulation when developing therapeutic interventions for MDD.

Metastatic disease remains the most important prognosis factor in HGOS. Improvements in surgical procedures and reduction in treatment-related mortality were observed. Survival after multiple relapses remains poor; we define figures to be used for benchmarking in clinical trials. BTN3A2 is a potential therapeutic target.

BTN3A2 interacted with MFGE8 to alleviate PE by promoting ferroptosis and inhibiting angiogenesis. Therefore, it may serve as a potential therapeutic target for the diagnosis and treatment of PE.

In this study, we identified 3 tier-one genes (MCM6, C4B, CTC-463A16.1), 7 tier-two genes (C4A, HLA-DRB9, LIMS2, LINC00654, MYO7B, SIGLEC5, TIE1), and 13 tier-three genes (AC007743.1, AC147651.4, ALDH2, BTN3A2, BTNL9, CCR1, GIPC3, HLA-DQB1, ICAM5, LIMD1, PM20D1, RP11-302L19.3, RP11-768F21.1).

Mechanistically, BTF3 plays an oncogenic role by regulating the transcriptional expression of PDCD2L, which promotes proliferation and inhibits apoptosis of HCC cells by restraining the p53 pathway. In conclusion, our results suggest that BTF3 induces malignant progression of HCC by acting as a transcription factor that promotes the transcription of PDCD2L and influences the p53 pathway and that the BTF3/PDCD2L/P53 axis may be a future therapeutic strategy for HCC patients.

Through assessment of ADMET properties and binding ability of receptor-ligand, 15 antagonists and 25 agonists of matched drug-like chemicals showed therapeutic effects on target genes. On the basis of causal relationship, docking score and ADMET evaluation, these hit targets and drug-like compounds yield new directions for the development of potent therapeutic agents in melanoma patients.