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
- Chronic inflammation has long been associated with cancer initiation, yet the mechanisms linking sustained immune activation to an immune-permissive tumor microenvironment remain incompletely defined. Prevailing explanations such as immune exhaustion (IEX) or free radical mediated tissue damage, fail to account for the active state of immune tolerance, a process driven by potent negative feedback loops that systematically suppress host effector responses. - Source: PubMed
Publication date: 2026/08/11
Mazzio Elizabeth ABarnes Andrew SBadisa Ramesh BDarling-Reed Selina FSoliman Karam F A - Newcastle disease virus (NDV) can spread across regions via migratory wild birds, posing potential threats to livestock breeding and public health security. Systematic information on the genetic characteristics, immunoregulatory functions, and antiviral activity of IFN-γ in the migratory wild bird remains limited. - Source: PubMed
Publication date: 2026/08/11
Chang HuaDai FeiyanCheng HonglinChen YiZhao XiaotongRen ShengjieZhang HongliDuan BofangXiang XunDuan Gang - 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