IRF1 expression

Thus, here we present the first report of IRF11 orchestrating the activation of MDA5 transcription by binding to the ISRE of MDA5 promoter and forming a transcriptional complex with p300 and Pol II. Our results revealed an ancient regulatory mechanism of MDA5 in lower vertebrates, providing insights into its function and evolution.

These findings suggest that BAP1 may function as a tumor suppressor by regulating the tumor microenvironment and immune response. Our study also establishes the rationale for therapeutic strategies to restore tumor-specific MHC-II expression and enhance immunotherapy outcomes at epigenetic levels in B cell lymphoma treatment.

These findings highlight the adaptive role of IRF elements in enhancing, among other things, the bat immune system, potentially improving their resilience and efficacy. Our study not only provides new genetic insights into bats but also underscores the remarkable molecular evolution within this unique group of mammals.

Together, these findings indicate the existence of a molecular context linking dedifferentiation and IFNγ signaling in melanoma which may lead to immune evasion. Additionally, the variability in PD-L1 expression among MITFlow and MITFhigh cells suggests that high IFNγ-induced PD-L1 expression associates with enhanced inflammatory gene expression. These results imply that modulating melanoma differentiation may help shape IFNγ responsiveness.

Together, these results demonstrate that CLEC12B plays an important function in the human skin, bridging innate and adaptative immunity. This mechanism is of great interest as IFNγ and cellular recruitment are key initial steps involved in inflammation of many skin pathologies, making this receptor an interesting therapeutic target.

Knockdown of IL-6 or blockade with IL-6 receptor McAb attenuated MYD88 upregulation by SP1/IRF1 signaling in EOC cells with MYD88high (P < 0.001). In conclusion, CpG hypomethylation at the proximal promoter/5'UTR contributes to MYD88 upregulation in EOC via IL-6/SP1/IRF1 pathway.

Our findings demonstrate the crucial role of TNF-α1 in antiviral defense mechanisms in zebrafish and provide valuable insights into the functional conservation of TNF-α signaling across vertebrate species. This knowledge may contribute to the development of strategies to combat viral diseases in fish.

Immunohistochemistry showed HMGB3 expression correlated with ferroptosis-associated proteins and IRF1 expression in breast cancer tissue. HMGB3 contributes to anti-PD-1 resistance by inhibiting IFN-γ-driven ferroptosis in TNBC which suggested HMGB3 is a potential co-target with anti-PD-1 therapy for TNBC.

Our work identified three subtype-specific transcription factors that regulate three polyamine metabolism genes in high-risk breast cancer subtypes and the tumor microenvironment. Our results deepen the understanding of the role of polyamine metabolism in breast cancer and may help the clinical therapy of advanced breast cancer subtypes.

IHC indicated that IRF1 was downregulated in NSCLC tissues. Our study provides comprehensive bioinformatic analysis and experimental verification of IRF1, suggesting its potential as a prognostic biomarker in cancer.

Of note, it was discovered that an increase in CXCL10 was positively associated with improved survival in CRC. These findings strongly suggest that IRF1 serves as a key transcription factor for CXCL10, highlighting its potential as a therapeutic target for CRC.

Furthermore, in mouse syngeneic tumor models, Ythdf1 depletion in cancer cells resulted in reduced tumor growth and increased tumor-infiltrating lymphocytes, which are attributed to the augmentation of IFN-γ signaling. Collectively, these findings highlight how YTHDFs modulate cancer immunity by influencing IFN-γ signaling through IRF1 regulation, suggesting their viability as therapeutic targets in cancer immunotherapy.