IRF2
- Known as:
- IRF2
- Catalog number:
- 000437A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- IRF2
Related genes to: IRF2
- Gene:
- IRF2 NIH gene
- Name:
- interferon regulatory factor 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 4q35.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-05-09
- Date modifiied:
- 2016-01-15
Related products to: IRF2
Related articles to: IRF2
- KRAS-mutant colorectal cancer (CRC) exhibits an aggressive metastatic phenotype, largely driven by TGFβ-induced epithelial-mesenchymal transition (EMT). However, the downstream effectors mediating TGFβ-driven metastasis in this context remain incompletely defined. This study identifies interferon regulatory factor 2 (IRF2) as a key metastasis suppressor and direct transcriptional repression target of TGFβ-SMAD2/3 signaling. IRF2 expression is markedly downregulated at invasive tumor fronts, showing a significant inverse correlation with p-SMAD2 levels and advanced metastatic stage. Single-cell trajectory analysis reveals temporal IRF2 suppression precisely coinciding with TGFβ/EMT program activation during metastatic progression. Mechanistically, SMAD2/3 complexes directly bind the IRF2 promoter to mediate repression, and IRF2 overexpression effectively reverses TGFβ1-induced invasive phenotypes in vitro. Pharmacological TGFβR1 inhibition restores IRF2 expression, slowing tumor progression and extending survival in the KRAS-driven iKAP mouse model. Furthermore, IRF2 reconstitution potently inhibits CRC cell invasion and metastasis by transcriptionally repressing EMT-related genes and enhancing anti-tumor immunity, characterized by increased CD8 T-cell infiltration and reduced regulatory T cells (Tregs). While active in various CRC contexts, the TGFβ-SMAD2/3-IRF2 axis is particularly critical in KRAS-mutant CRC, where IRF2 loss acts as a functional second hit to accelerate dissemination. These findings uncover a TGFβ-SMAD2/3-IRF2 axis governing EMT and metastatic dissemination, positioning IRF2 restoration as a promising therapeutic strategy for aggressive KRAS-mutant CRC. - Source: PubMed
Publication date: 2026/04/14
Shu FengZhang TaoChen XiaoningLu GuohaoGuo ShiZhang YaxinHuang ChengmeiLiao WentingAlan Wang Y - Recent findings emphasize that IRF1 and IRF2 play distinct roles in gene regulation, particularly through chromatin remodeling during antiviral responses. Our current data extend this by revealing that IRF1 directly targets TNS3, a key regulator of renal stress, fibrosis, and the aging process. We identify a mechanistic parallel between the IRF1-TLR3 and IRF1-TNS3 pathways, proposing that targeting the IRF1-mediated modulation of TNS3 could offer a fresh therapeutic approach for kidney injury. - Source: PubMed
Publication date: 2026/03/19
Huang Chien-WeiWen Chen-YuehHsu Yu-JueiLi Chia-Jung - Type I interferon (IFN-I) and interferon-γ (IFNγ) are central regulators of antiviral immunity, yet how they cooperatively govern CD8 T cell fate during chronic infection remains unresolved. Here, we uncover a previously unrecognized, spatially encoded interferon circuit that actively constrains progenitor exhausted CD8 T cells (Tpex) during chronic LCMV infection. Persistent IFN-I signaling indirectly restricts Tpex expansion by enforcing their sequestration within PDL1-rich B cell niches of lymphoid tissue and by suppressing T cell-derived IFNγ. Blockade of IFN-I signaling enables Tpex migration into T cell zones of splenic follicles driving IFNγ production, which in turn sustains PDL1 expression on myeloid cells to re-impose local inhibitory pressure. Combined IFN-I and IFNγ blockade disrupts this feedback, promoting coordinated niche redistribution of Tpex and checkpoint remodeling that drives robust Tpex expansion. Single-cell transcriptomics reveal that this layered IFN-I-IFNγ interplay establishes a regulatory balance that constrains Tpex proliferation while preserving effector-like transcriptional programs in their progeny effector CD8 T cells, ultimately preventing premature terminal differentiation. Thus, interferons orchestrate the coordinated T cell-myeloid regulatory circuit that integrates tissue organization, cytokine feedback, and checkpoint control to regulate CD8 T cell exhaustion during chronic infection. - Source: PubMed
Publication date: 2026/03/03
Liu SiranElsaesser Heidi JQuevedo ReneAbd-Rabbo DialaBertol Bruna CXu WenxiLiu Melissa Yi RanLukhele SabeloLamorte SaraMcGaha Tracy LBrooks David G - Dengue fever challenges public health worldwide. The numerous factors associated with dengue fever severity and mortality risk include host characteristics such as patient age, comorbid conditions, previous dengue virus (DENV) infections, and biochemical biomarkers. Type I IFNs are essential cytokines in orchestrating innate and adaptive immune responses against viral invasion, and their regulation is mediated by IRF-2, which prevents excessive IFN expression. In vitro studies have shown DENV evasion strategies that affect IFN-I production but few have considered the in-situ interrelationship between IFN-I and the virus. This study aims to find elements of innate immunity that induce the anti-viral response and their correlation with the detected alterations in liver lesions. Liver specimens from individuals who died due to dengue were selected according to clinical and laboratory data and serological diagnosis. The specimens were subjected to histological and immunohistochemical evaluation of cells expressing IFN-I, RIG-1, IRF-2, and STING. Viral antigens were detected by an anti-DENV. A high number of cells expressed RIG-1 and IRF-2 when compared to IFN-I and STING. In severe cases of dengue, DENV may play a role in its pathogenesis with properties that induce non-effective immune responses. The virus can evade effective immune responses by impairing the early activation of innate immunity. This immune dysregulation may contribute to the progression of more severe manifestations and seems to play a role in the pathogenesis of hepatic involvement. - Source: PubMed
Publication date: 2026/03/02
Pagliari CarlaMarcoli Geovanna MenezesKanashiro-Galo LucianeMello Evandro Sobroza deCarvalho Leda Viegas dePenny RicardoQuaresma Juarez SimõesVasconcelos Pedro Fernando da CostaSotto Mirian Nacagami - Emerging evidence suggests a potential association between high selenium (Se) exposure and the development of type 2 diabetes mellitus (T2DM), a condition often associated with chronic low-grade inflammation. Pyroptosis, a form of programmed cell death characterized by the cleavage and activation of GSDMD by Caspases, has been implicated in T2DM. As an interferon regulatory factor, IRF2 plays a key role in regulating Caspase-GSDMD-mediated pyroptosis. However, the role of IRF2 in Se-induced islet cell pyroptosis and its contribution to T2DM development remain unclear. This study investigates the relationship between Se exposure and T2DM, focusing on the molecular mechanisms through which IRF2 mediates pyroptosis. Our findings show that Se accumulates in the serum of diabetic mice, exacerbating hyperglycemia, reducing serum insulin levels, and triggering pancreatic tissue atrophy and inflammation. Additionally, Se exposure leads to its accumulation in INS-1 cells, decreasing cell viability and impairing insulin secretion. Treatment with the pyroptosis inhibitor disulfiram (DSF) effectively suppressed Se-induced GSDMD expression, GSDMD-N cleavage, and the production of apoptosis-associated speck-like protein (ASC) and interleukins (IL)-18, confirming that Se exposure triggers pyroptosis in pancreatic islet cells. Both in vivo and in vitro experiments consistently demonstrate that Se exposure induces pyroptosis through activation of the IRF2/Caspase-4/GSDMD signaling pathway. Notably, lentivirus-mediated silencing of IRF2 significantly suppressed Se-induced pyroptosis. In conclusion, our study suggests that accumulated Se exposure promotes the progression of T2DM via the IRF2/Caspase-4/GSDMD-mediated pyroptosis pathway. Moreover, targeting IRF2 expression may effectively alleviate Se-induced pancreatic β-cell damage, providing a promising therapeutic target for the prevention and treatment of T2DM. - Source: PubMed
Publication date: 2026/02/22
Wei LanchengLi ZhenShan JunhaoChen XiaolangZhou HuijiaoZhong JinYang YongmeiChi JinfanZhang BeisiqiLiang HengweiMo ZhidongXie LinfeiLin RuiLv YingnanLi ShaojunZhang Haiying