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    GENE:

    IFI16 (Interferon Gamma Inducible Protein 16)

    i
    Other names: IFI16, Interferon Gamma Inducible Protein 16, IFNGIP1, Interferon-Inducible Myeloid Differentiation Transcriptional Activator, Gamma-Interferon-Inducible Protein 16, PYHIN2, Interferon-Gamma Induced Protein IFI 16, IFI16 Beta Isoform, Ifi-16
    10d
    Enhancing Oncolytic Adenovirus Replication by Early Region 1A Protein-Mediated Degradation of E1A Binding Protein p300. (PubMed, MedComm (2020))
    In this study, OAd can reduce p300 expression by promoting its ubiquitination via E1A, thereby enhancing viral replication and cell cytotoxicity. Therefore, this study can provide a biomarker for screening patients who are sensitive to OAd and new ideas for clinical tumor treatment.
    Journal
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    EP300 (E1A binding protein p300) • STING (stimulator of interferon response cGAMP interactor 1) • IFI16 (Interferon Gamma Inducible Protein 16) • IFNB1 (Interferon Beta 1)
    1m
    Superenhancer-driven SMC4 promotes myeloma growth by epigenetically enhancing IFI16-dependent STING signaling. (PubMed, Apoptosis)
    Our findings uncover a novel regulatory circuit involving SMC4 and the IFI16-STING signaling axis that promotes myeloma growth. Targeting this epigenetic network may hold therapeutic potential to intervene in myeloma progression and improve patient outcomes.
    Journal
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    IFI16 (Interferon Gamma Inducible Protein 16)
    2ms
    RRM1 inhibition sensitizes lung adenocarcinoma to decitabine treatment. (PubMed, Cell Death Dis)
    RNR inhibition led to increased incorporation of DAC into genomic DNA by reducing the availability of dCTP. These findings nominate the promising combination therapy of DAC and RNR inhibitors as being ripe for further clinical translation.
    Journal
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    RRM1 (Ribonucleotide Reductase Catalytic Subunit M1) • IFI16 (Interferon Gamma Inducible Protein 16)
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    decitabine
    3ms
    STING activation by teniposide: a potential direct mechanism beyond cGAS stimulation. (PubMed, Front Immunol)
    These findings suggest that Teniposide activates STING through a previously unrecognized, cGAS-independent mechanism, while retaining potential for canonical cGAS-STING stimulation. Our combined computational and experimental evidence supports repurposing Teniposide as a STING agonist, highlighting new therapeutic possibilities for innate immune stimulation.
    Journal
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    STING (stimulator of interferon response cGAMP interactor 1) • CGAS (Cyclic GMP-AMP Synthase) • IFI16 (Interferon Gamma Inducible Protein 16) • IFNB1 (Interferon Beta 1)
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    Vumon (teniposide)
    3ms
    The ever-expanding role of IFI16 in the anti-viral innate immune response. (PubMed, Immunol Lett)
    Consistent with these antiviral roles, many viruses have evolved both destructive (IFI16 degradation) and non-destructive mechanisms to evade IFI16. This review summarizes the current understanding of how IFI16 mediates broad antiviral restriction and how diverse viruses subvert this role to facilitate their replication.
    Review • Journal
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    IFNG (Interferon, gamma) • STING (stimulator of interferon response cGAMP interactor 1) • IL18 (Interleukin 18) • CGAS (Cyclic GMP-AMP Synthase) • IFI16 (Interferon Gamma Inducible Protein 16) • IL1B (Interleukin 1, beta)
    3ms
    IFI16 senses and protects stalled replication forks. (PubMed, Mol Cell)
    IFI16 acts directly at stalled replication forks to protect nascent DNA from degradation by the nucleases MRE11, EXO1, and DNA2. Furthermore, IFI16 is required for the interferon-mediated rescue of fork protection in BRCA-deficient cells, highlighting the critical role of IFI16 in the crosstalk between innate immunity and fork protection during replication stress.
    Journal
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    BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • IFNG (Interferon, gamma) • BRCA (Breast cancer early onset) • STING (stimulator of interferon response cGAMP interactor 1) • MRE11A (MRE11 homolog, double strand break repair nuclease) • IFI16 (Interferon Gamma Inducible Protein 16) • DNA2 (DNA Replication Helicase/Nuclease 2)
    3ms
    A bortezomib resistance-related gene signature predicts prognosis, with ARID5B downregulation associated with poor overall survival in multiple myeloma. (PubMed, Discov Oncol)
    The BRGs signature is a reliable biomarker for predicting the prognosis of MM and helps optimize clinical decision-making for treatment, and identifies key gene ARID5B downregulation as an adverse prognostic factor in multiple myeloma.
    Journal • Gene Signature
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    LTBP1 (Latent-transforming growth factor beta-binding protein 1) • CRIP1 (Cysteine Rich Protein 1) • IFI16 (Interferon Gamma Inducible Protein 16) • ARID5B (AT-Rich Interaction Domain 5B)
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    bortezomib • doxorubicin hydrochloride • etoposide IV
    4ms
    GBP1 as a machine learning-prioritized biomarker and therapeutic target for epstein-barr virus-induced clear cell renal cell carcinoma: multi-omics causal validation. (PubMed, Int J Surg)
    This work reveals a causal relationship between EBV infection and ccRCC pathogenesis, establishing GBP1 as a top-priority candidate molecule through a multi-level, multi-dimensional evidence framework. Drug prediction and molecular docking suggest finasteride as a potential inhibitor of GBP1, offering new strategies for the precise prevention and treatment of ccRCC.
    Journal
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    GBP5 (Guanylate Binding Protein 5) • GBP1 (Guanylate Binding Protein 1) • IFI16 (Interferon Gamma Inducible Protein 16) • IL12RB1 (Interleukin 12 Receptor Subunit Beta 1) • RECQL (RecQ Like Helicase)
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    finasteride
    4ms
    Multi-omics highlights the impacts of cryptorchidism history on immune microenvironment variation in TGCT. (PubMed, Discov Oncol)
    We revealed unique molecular pathways in TGCT samples with cryptorchidism history and identified tumor-related features in cryptorchidism accumulation. Cryptorchidism history significantly remodels the immune microenvironment of TGCT.
    Journal
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    IFI16 (Interferon Gamma Inducible Protein 16)
    4ms
    METTL14 Regulates the Expression of Genes Related to Interferon, Interleukin and MHC Class I in Nasopharyngeal Carcinoma Cells. (PubMed, Cancer Med)
    These findings demonstrate, for the first time, that METTL14 modulates the expression of genes related to TNF, IFN, IL, and MHC class I in NPC, proposing a novel role for METTL14 in linking inflammation with cancer, a function that has not been fully elucidated.
    Journal
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    HLA-A (Major Histocompatibility Complex, Class I, A) • IL6 (Interleukin 6) • TNFA (Tumor Necrosis Factor-Alpha) • CXCL10 (Chemokine (C-X-C motif) ligand 10) • IL7R (Interleukin 7 Receptor) • TNFRSF9 (TNF Receptor Superfamily Member 9) • HLA-B (Major Histocompatibility Complex, Class I, B) • IL32 (Interleukin 32) • CD40LG (CD40 ligand) • IFI16 (Interferon Gamma Inducible Protein 16) • IL1B (Interleukin 1, beta) • IL7 (Interleukin 7) • PSMA2 (Proteasome 20S Subunit Alpha 2) • PSMC6 (Proteasome 26S Subunit, ATPase 6) • PSMD1 (Proteasome 26S Subunit Non-ATPase 1) • HLA-C (Major Histocompatibility Complex, Class I, C) • METTL14 (Methyltransferase 14) • TNFRSF12A (TNF Receptor Superfamily Member 12A)
    5ms
    FAM135B Deficiency Inhibits Cytotoxic T-Cell Activity in Triple-negative Breast Cancer by Blocking the IFI16-dependent STING Pathway. (PubMed, Cancer Immunol Res)
    These findings reveal that FAM135B regulates the IFI16-dependent STING pathway and subsequent immune activation. FAM135B may represent a potential predictor of ICB therapeutic responses for TNBC patients.
    Journal
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    IFI16 (Interferon Gamma Inducible Protein 16) • TRIM21 (Tripartite Motif Containing 21)