IRF5 (Interferon Regulatory Factor 5)

Our findings identify UDP as a potent immunomodulatory metabolite that restricts monocyte proliferation while promoting differentiation into dendritic-like cells with enhanced phagocytic capacity. UDP engages complex transcriptional programs that integrate innate activation with adaptive immune regulation, highlighting its potential role in immune homeostasis and inflammation control.

It was found that it regulated cellular responses along with apoptotic mechanisms in cells without developing resistance in suppressing tumor growth by making changes on Atf2, Casp8, Bcl2 and Irf5 genes and proteins. As a result, the biotechnological drug potential of TRAIL was discovered in an aptamer-bound nanosystem for the treatment of triple-negative breast cancer and innovative applications for clinical use.

Furthermore, the incubated CT-26 cell line with conditioned medium of BBE treatment groups suppresses proliferation and impedes migration of cancer cells. we found that BBE-treated macrophages possess an M1-like phenotype and inhibit the proliferation and motility of CT-26 cancer cells.

Regulatory network analysis revealed that the transcription factors ETV5, IRF5, IRF7, RORB, RORC, and SMAD1 drive inflammatory and profibrotic signatures via the IL-17, JAK-STAT, and TGF-β pathways. This study identifies monocytes as central orchestrators of immune dysregulation in ASS-ILD, highlighting IFN/TNF signaling and associated transcriptional regulators as therapeutic targets.

ISL may inhibit TNBC progression by downregulating IRF5 and interfering with SLC7A5/IDO1-mediated tryptophan metabolic reprogramming, suggesting a potential therapeutic mechanism for TNBC treatment.

Notably, risperidone (SM-2) emerged as a potential inhibitory regulator capable of disrupting the cascade effects mediated by the GDF15-GFRAL axis, underscoring its therapeutic relevance. This study identifies the GDF15-GFRAL signaling axis as a critical regulator of oxidative stress and immune evasion in HNSCC and demonstrates that the novel small-molecule SM-2 effectively targets this pathway, highlighting its potential as a promising therapeutic strategy.

MCTN is validated as a cancer vaccine platform utilizing full-length antigens, generating robust immune responses with broad HLA-haplotype coverage. Finally, using a payload encoding constitutively active interferon regulatory factor 5 (IRF5), MCTN is found to suppress solid tumor growth and modulate the TME by improving CD8+ T-cell infiltration while depleting immunosuppressive cells.

Finally, in vivo studies indicated that M. tuberculosis-mediated increase of MafB expression was responsible for the exacerbation of M. tuberculosis infection. Thus, our results provide a functional view of MafB as a cytokine regulator as well as novel insights into host factors involved in TB susceptibility.

The present study provides evidence supporting a causal link between HCV infection and the development of kidney cancer.

Extensive DNA repair gene defects, primarily complex SVs detectable by long reads, were observed and highly possibly associated with poor survival. These findings underscore the potential of long-read sequencing for uncovering clinically relevant mutations in NPC.

Our study highlights the association between rs3757385 (G allele) and high plasmatic NOx levels as good prognostic factors in UBC.

MMRN1 is a critical BTSC-related biomarker that contributes to GBM progression by enhancing tumor stemness and modulating the immune microenvironment. Targeting MMRN1 May represent a promising therapeutic approach for GBM treatment.