Ask about this productRelated genes to: IRF7 antibody
- Gene:
- IRF7 NIH gene
- Name:
- interferon regulatory factor 7
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-13
- Date modifiied:
- 2019-04-23
Related products to: IRF7 antibody
Related articles to: IRF7 antibody
- The clinical utility of doxorubicin (DOX) is severely limited by dose-dependent cardiotoxicity, for which effective interventions remain scarce. Huangqi Guizhi Wuwu Decoction (HGWD) shows promising cardioprotective potential, but its mechanisms against DOX-induced cardiotoxicity (DIC) remain unexplored. This study explored the molecular mechanisms using an integrated metabolomics and transcriptomics approach. We identified 57 compounds in HGWD by liquid chromatography ion trap time-of-flight mass spectrometry (LC-IT-TOF/MS), and quantified five representative compounds for standardization. Mice were randomized into six groups: control, DOX (10 mg/kg × 2), DOX + low-dose HGWD (7 g/kg/d), DOX + high-dose HGWD (14 g/kg/d), DOX + dexrazoxane (100 mg/kg × 2), and HGWD (14 g/kg/d) alone. HGWD effectively alleviated cardiac dysfunction and reduced serum injury markers, with the high-dose group demonstrating efficacy comparable to the positive control drug, dexrazoxane. Subsequently, multi-omics profiling was performed on heart tissues from the control, DOX, and DOX + high-dose HGWD groups. Metabolomics identified 31 differential metabolites, highlighting energy metabolism restoration (e.g., acylcarnitines, citric acid) and inflammatory mediator modulation (e.g., arachidonic acid). Transcriptomics uncovered 37 genes enriched in innate immunity (e.g., Irf7, Isg15) and apoptosis (e.g., Bax, Cdkn1a). Network analysis constructed a core regulatory module, pinpointing CDKN1A as a potential mediator. Validation experiments confirmed that HGWD suppressed DOX-induced CDKN1A upregulation in mouse hearts. Furthermore, in H9c2 cells, HGWD mitigated DOX-induced apoptosis and inflammation, exhibiting cytoprotection comparable to pifithrin-α, a specific p53 inhibitor. In summary, HGWD protects against DIC by modulating a multi-target network and the suppression of CDKN1A represents a key underlying mechanism. - Source: PubMed
Publication date: 2026/08/21
Hou QianYu XinyueWu KeChen SilingMao XinQian XinyingLi ChangjinSheng LidanWang RuipingHuang Yin - Aging is known to alter innate immune function, increasing susceptibility to viral infections, yet its specific effects on influenza B virus (IBV) infection remain poorly characterized. To address this gap, we developed a preclinical mouse model using a clinically relevant IBV strain Inf B/Phuket/3073/2013 to compare innate immune responses between young adult and aged mice, with a particular focus on age-related transcriptional and proteomic alterations in lung during infection. Bulk RNA sequencing and proteomics analysis of lung tissue harvested post-infection revealed distinct age-dependent transcriptional profiles. Bulk RNA-seq analysis identified 1,350 differentially expressed genes (DEGs), of which 824 exhibited an aged-biased expression pattern and were significantly upregulated in the lungs of influenza B virus-infected aged mice. Functional enrichment of these DEGs indicated perturbations in innate immune signaling, apoptosis, and pathways related to cellular stress and DNA damage in aged mice. There are several differentially expressed proteins that have been identified in young adult and aged influenza B infection. Among these differentially expressed proteins, some commonly co-expressed proteins have a role in virus entry, signaling pathways, and interferon response. Real-time PCR analysis confirmed altered expression of key innate immune genes, including Toll-like receptors (TLRs), interferon regulatory factors (IRF7 and IRF9), key antiviral genes (IFIT -2, IFIT-3 and STAT-1) and type I and II interferons (IFN-α, IFN-β, IFN-γ). Notably, young adult mice exhibited a more coordinated and robust activation of antiviral pathways, whereas aged mice demonstrated delayed and aberrant immune responses, characterized by excessive inflammation and impaired interferon signaling. - Source: PubMed
Publication date: 2026/08/19
Saxena ShikhaKaur GurleenVishwakarma PreetiKumar VarunKumar AmitOmpal SoniaKumar SatishSingh SarjeetChauhan AkankshaChaudhuri SusmitaMalla Waseem AkramSamal Sweety - Acute myeloid leukemia/myelodysplastic syndromes (AML/MDSs) carrying p53 mutations are refractory to various standard therapies. Arsenic trioxide (ATO) may be effective in restoring function to p53 structural mutants. Here, we report that mutant p53 rescued by ATO treatment strengthened interferon responses triggered by the DNA hypomethylating agent decitabine by transactivating () directly. Decitabine also increased the transactivation activity of ATO-rescued mutant p53 by inducing p53-serine-20 phosphorylation and blocking p53-inhibitory mouse double minute 2 homolog (MDM2). ATO and decitabine together killed p53-mutant AML cells and suppressed tumor growth in cell line-derived xenografts. In a first-in-human pilot clinical trial for testing the combination of ATO and decitabine (PANDA-T0 trial, NCT03855371), which enrolled five patients with AML/MDS harboring p53 structural mutations, the ATO and decitabine regimen produced manageable adverse events, and four of the five treated patients achieved complete remission at the level of the bone marrow, associated with p53 activation and interferon response. In 103 p53-mutant patients whose samples were deposited in Ruijin AML/MDS sample repository, 48 distinct p53 missense mutants were identified, 21 of which were classified as ATO and decitabine regimen applicable because of their competencies in activating p53 and interferon responses upon cotreatment. This study establishes an alternative treatment regimen for patients with p53-mutant AML/MDS and provides a proof-of-concept framework for p53-targeted therapy that differentiates between p53 mutations. - Source: PubMed
Publication date: 2026/08/12
Song HuaxinChen XinjieXiao ShujunWu JiaqiDai YutingWu WenWu YuWeng XiangqinSong JiachunYan NiYe ChenjingShi FangfangCui JingyiZheng DerunZhang HesongTan KaiChen XueqinZhang SujiangWu JialeLu Min - Systemic type I interferon (IFN-I) and pro-inflammatory cytokine responses are critical for limiting mosquito-borne RNA virus viral replication and disease, yet mechanisms initiating these responses and their linkage to viral tropism for lymphoid tissues are poorly understood. Here, we reveal that virus-cell interactions and specific host signaling pathways in lymphoid tissues are determinants of systemic cytokine induction. Using Venezuelan equine encephalitis virus (VEEV) mutants with defined lymph node (LN) tropism in mice, we show that VEEV LN infection positively associates with systemic IFN-I and other proinflammatory cytokine induction. Maximal responses require coordinated activation of multiple IRF7-dependent Toll-like receptor and RIG-I-like receptor pathways. Combining targeted cell depletion and Visium HD spatial transcriptomics viral gene quantitation, we uncover a spatiotemporal, biphasic innate immune response to VEEV infection, with initial cytokine induction driven by VEEV replication in dendritic cell and monocyte/macrophage subtypes within the LN subcapsular sinus. Surprisingly, active virus replication is curtailed in this LN compartment before 16hpi, when cytokine induction becomes dominated by non-VEEV-replicating bystander cells including plasmacytoid dendritic cells. These findings have direct implications for intervention against viral diseases characterized by lymphoid infection and subsequent spread to sites of terminal disease. - Source: PubMed
Publication date: 2026/08/12
Jacoby Melaina LSun ChengqunFarren Jessica LMarti Michelle MLee Alyssa LDonovan ThomasKlein Robyn SRajasundaram DhivyaaKlimstra William B - Mammalian reovirus µ2 antagonizes type I interferon (IFN) signaling and is associated with nuclear hyperaccumulation of IRF9. We tested whether µ2 residue 208, which determines strain-specific IFN-β repression and modulation of host cell mRNA splicing, also controls IRF9 relocalization and whether the splicing factor SRSF2 is required. Recombinant and mutant viruses showed that T1L-like Pro208 is required and sufficient for IRF9 nuclear accumulation in L929 cells. In addition, SRSF2 depletion reduced IFN-mediated induction of and , but not , and abolished T3D-S208P-induced IRF9 nuclear accumulation. Thus, reovirus-induced IRF9 relocalization requires both µ2 residue 208 and host SRSF2. - Source: PubMed
Publication date: 2026/07/27
Rivera-Serrano Efraín E