Ask about this productRelated genes to: IFIT2 Blocking Peptide
- Gene:
- IFIT2 NIH gene
- Name:
- interferon induced protein with tetratricopeptide repeats 2
- Previous symbol:
- IFI54, G10P2
- Synonyms:
- IFI-54, ISG-54K, cig42, GARG-39
- Chromosome:
- 10q23.31
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-06
- Date modifiied:
- 2015-11-27
Related products to: IFIT2 Blocking Peptide
Related articles to: IFIT2 Blocking Peptide
- We constructed a gene coexpression network to uncover central key genes related to Sjögren's disease (SjD), and investigated the clinical significance of bone marrow stromal antigen 2 (BST2) in SjD. - Source: PubMed
Publication date: 2026/04/09
Ren TianZhou XinZhou EryeLiu CuipingWu JianChang XinChen Weichang - Interferon-induced proteins with tetratricopeptide repeats (IFITs) are RNA-binding effectors that restrict infection by diverse RNA viruses. Among the IFIT family, how IFIT3 recognizes RNA remains the least understood. Here, we identify IFIT3 as preferentially associating with N6-methyladenosine (m⁶A)-modified hepatitis C virus (HCV) genomic RNA and host transcripts to restrict HCV infection. IFIT3 cellular RNA binding sites and m⁶A sites, mapped transcriptome-wide by HyperTRIBE-seq during HCV infection, showed significant overlap. This m⁶A preference was further supported by findings that IFIT3 binding sites significantly overlapped those of established m⁶A-binding proteins; that inhibiting m⁶A installation reduced IFIT3 association with m⁶A-modified HCV RNA and cellular transcripts; that IFIT3 co-purified more efficiently with m⁶A-modified short RNA probes than with unmodified controls; and that mutating m⁶A consensus motifs in the HCV genome reduced IFIT3 association with viral RNA. Structure-function analyses identified two regions required for RNA probe binding: tetratricopeptide repeat domains 1-2 (TPR1-2) and a previously uncharacterized predicted helical hairpin between TPRs 6 and 7. In infected cells, the helical hairpin was required for IFIT3 association with HCV RNA but dispensable for interactions with other IFIT proteins. Conversely, TPR1-2 was dispensable for HCV RNA binding but essential for IFIT2 interaction, establishing that these functions are structurally separable. Loss of either region diminished antiviral activity, as indicated by increased levels of HCV RNA in clarified supernatants. Consistent with models of m⁶A-linked restriction of late stages of infection, extracellular HCV RNA showed reduced m⁶A and decreased IFIT3 association relative to intracellular RNA. Together, these findings define an m⁶A-linked mechanism by which IFIT3 engages viral RNA and reveal an unexpected role for m⁶A in antiviral effector function. - Source: PubMed
Publication date: 2026/03/26
Thompson MatthewPark MoonheeSchlamowitz Netanya SLanahan Matthew RNam YunsumHorner Stacy M - Gastric cancer (GC) remains a leading cause of cancer-related deaths worldwide. Circular RNAs (circRNAs) have been increasingly recognized for their role in GC progression, particularly by acting as competing endogenous RNAs (ceRNAs) that regulate miRNA activity. This study aimed to elucidate the regulatory mechanisms of circRNAs in GC.Differentially expressed circRNAs, miRNAs, and mRNAs were identified from Gene Expression Omnibus datasets. Functional enrichment analysis of differentially expressed genes was performed using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis. A circRNA-miRNA-mRNA regulatory network was constructed based on predicted interactions. The PT-qPCR was used to detect the expression level of circRNAs in GC specimens and cell lines. The effects of hsa_circ_004228 on the GC cell functions were detected by CCK-8, Colony formation, and Transwell assay.The ceRNA network consisted of 9 core circRNAs, 10 core miRNAs, and 23 core mRNAs. Pathway analysis revealed that these mRNAs were primarily enriched in cancer-related pathways, including PI3K-Akt signaling, p53 signaling, and ECM-receptor interaction. Prognostic analysis indicated that high IER5L expression correlated with better survival, whereas high FNDC1, HTRA1, IFIT2, NDUFA4L2, and SERPINE1 expression correlated with poorer prognosis. A ceRNA prognostic subnetwork was established, incorporating 5 circRNAs (hsa_circ_0007094, hsa_circ_0007613, hsa_circ_0008768, hsa_circ_0006089, and hsa_circ_004228) and 4 miRNAs (hsa-miR-765, hsa-miR-198, hsa-miR-125a-3p, and hsa-miR-486-5p) associated with these prognostic mRNAs. The expression levels of hsa_circ_0007094, hsa_circ_0004228, hsa_circ_0007613, hsa_circ_0008768, and hsa_circ_0006089 were significantly upregulated in gastric cancer tissues. Knockdown of hsa_circ_0004228 significantly inhibits the activity, proliferation, migration, and invasion of HGC27 and AGS cells.In conclusion, we identified key circRNAs, miRNAs, and mRNAs involved in GC progression and prognosis, constructing a ceRNA network that provides novel insights into GC pathogenesis. These findings may aid in identifying potential biomarkers for GC diagnosis and prognosis. - Source: PubMed
Publication date: 2026/03/20
Wen JunHe YaqinLiu ZijianLi RuyiZhang Cao - Ovarian clear cell carcinoma (OCCC) is a rare cancer type of significant relevance to East Asian women harboring critical unmet needs for novel therapeutic options. It is a histological subtype of ovarian cancer with distinct pathological features, molecular profiles, and biological functions. Diverse heterogeneity contributing from histopathological and multiomic molecular features has yet to be translated to guide clinical care. Here, we presented a proof-of-concept study to demonstrate the feasibility of applying deep spatial transcriptomic (ST) profiling of tumor samples from an advanced OCCC patient in the real-world setting, aiming to identify therapeutic options beyond standard-of-care. Matched primary ovarian and metastatic bladder tumor sections were profiled by using GeoMx Digital Spatial Profiling and Xenium In Situ platforms. The spatial architecture and neighborhood niches were identified from GeoMx Cancer Transcriptome Atlas (CTA) and Xenium 5K Human Pan Tissue and Pathways Panel. An immunosuppressive Wnt-activating tumor microenvironment (TME) was identified by GeoMx while a tripartite spatial relationship between SLC2A1+ hypoxic cancer cells, IFIT2+ inflammatory cancer cells, and MMP12+ dendritic cells linking towards metabolism and immune responses was identified by Xenium. Our deep ST profiling findings provided significant biological insights and demonstrated feasibility to make novel discoveries, one patient at a time. - Source: PubMed
Publication date: 2026/03/03
Le Thang TruongYang Alice Hsiang-KuoChen Ko-ChenChiu Yi-ChiaNecesario Sydney RechieMavuso Mqondisi FortuneTan Tuan ZeaTai Ya-TingLin Wei-ChouChiang Ying-ChengWei Lin-HungHuang Ruby Yun-Ju - sp., a marine microalga amenable to mass cultivation, possesses antiviral properties, partly attributed to chlorophyll a. However, the underlying antiviral mechanisms remain poorly characterized. In this study, we investigated the antiviral activity and mode of action of chlorophyll a derived from sp. by performing transcriptomic analyses on three experimental groups: untreated, uninfected cells; Zika virus (ZIKV)-infected cells; and chlorophyll a-treated, ZIKV-infected cells. Treatment with 5 µM chlorophyll a induced differential expression of genes associated with interferon-inducible antiviral responses. Gene ontology analysis revealed significant enrichment of biological processes such as "response to external stimulus" and "response to biotic stimulus." Notably, Venn diagram analysis of 130 differentially expressed genes (DEGs) demonstrated restoration of key interferon-stimulated genes, including interferon-induced protein with tetratricopeptide repeats (IFIT)1, IFIT2, IFIT3, and IFIT5, which was further validated by quantitative PCR and immunocytochemistry. These findings suggest that chlorophyll a from sp. exerts antiviral effects primarily through modulation of interferon-mediated pathways. See also the graphical abstract(Fig. 1). - Source: PubMed
Publication date: 2026/01/09
Kang NalaeKim Eun-ALee Yeon-JiHeo Seong-YeongHeo Jun-HoLee Won-KyuRyu Yong-KyunKim TaehoHeo Soo-Jin