Ask about this productRelated genes to: IFITM3 antibody
- Gene:
- IFITM3 NIH gene
- Name:
- interferon induced transmembrane protein 3
- Previous symbol:
- -
- Synonyms:
- 1-8U, DSPA2b
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-11
- Date modifiied:
- 2018-03-08
Related products to: IFITM3 antibody
Related articles to: IFITM3 antibody
- Interferon-induced transmembrane protein 3 (IFITM3) is an antiviral protein with emerging roles in regulating inflammatory pathways. Although much is known about the role of IFITM3 in mediating host antiviral defense, its contribution to systemic immune responses during critical infectious illnesses remains less understood. Here, we provide evidence that IFITM3 levels were significantly higher in cell free BAL fluid in septic patients with pulmonary infections and in circulating plasma extracellular vesicles (EVs) from critically ill septic patients compared to critically ill non-septic patients and healthy individuals. This study provides the first evidence of IFITM3's association with sepsis induced inflammatory responses and bacterial pulmonary infections, raising its potential as an agent of dysregulated immunity during systemic infection. - Source: PubMed
Das SrabaniSpitzer Carleen RConsiglio PaulExline Matthew CSarkar Anasuya - Orthoflaviviruses comprise genetically diverse mosquito-borne viruses responsible for a broad spectrum of human diseases. Although naturally circulating clinical isolates exhibit biological variability, the extent to which they generate distinct early epithelial innate immune responses remains incompletely understood. Here, we characterized five clinical orthoflavivirus isolates obtained in Oaxaca, Mexico, using human HaCaT keratinocytes as an in vitro model of early infection. Productive infection was assessed by immunofluorescence microscopy, immunostained focus appearance under isolate-optimized assay conditions, and infectious virus production, whereas host responses were evaluated by transcriptional profiling and quantitative whole-slide single-cell immunofluorescence. All isolates established productive infection and exhibited different viral replication profiles. Temporal transcriptional analyses revealed variable expression of antiviral (IFNβ, Mx1, OAS1, PKR, IFITM3, Viperin, and RANTES) and inflammatory (TNF-α, IL-8, and MCP-1) genes. Quantitative whole-slide analysis provided complementary evidence of variable STAT1 and NF-κB signaling activation across the analyzed isolates. Within this limited panel, viral replication was not consistently aligned with the selected transcriptional and signaling readouts, although the exploratory nature of these comparisons precludes establishing independence between these variables. Together, the virological, transcriptional, and imaging analyses revealed distinct multidimensional functional profiles across the isolate panel. Overall, these findings demonstrate functional heterogeneity among the analyzed clinical orthoflavivirus isolates and highlight integrated functional phenotyping as a useful framework for examining virus-host interactions beyond viral replication alone. - Source: PubMed
Publication date: 2026/07/27
Castro Jiménez Tannya KarenLopez Kelly Edwin AntonioCedillo-Barrón LeticiaGarcía-Cordero JulioCruz-Hernández Diego SaitDiaz Lima NallelySan Juan Luis José AlbertoCastillo Camacho Cruz CarlosPérez-Yépez Eloy AndrésIbarra-Moreno Cynthia DanielaFlores-Mejía Luis AngelAguilar-Ruíz Sergio RobertoMendoza-Rodríguez Mónica GTerrazas Luis IBustos-Arriaga José - The interferon-induced transmembrane (IFITM) protein family, including IFITM1, IFITM2, IFITM3, and the less-characterized IFITM5 and IFITM10, has emerged as a recurrent yet mechanistically complex group of players in cancer, reported as oncogenic in one setting and tumor-restraining in another, immunosensitizing in one context and immunotherapy-resistance-promoting in the next. Rather than treating this literature as contradictory, we argue it is unresolved, and we organize it around a four-axis framework defined by the interaction of member identity, interferon (IFN)-input quality, cellular compartment, and tumor milieu. - Source: PubMed
Liu ZheMeng JieLai ZengyanLi FuqiuLv Sha - Fish oogonial stem cells (OSCs) are vital for fish reproduction research and germplasm conservation, yet stable long-term in vitro culture of fish OSCs remains a major technical bottleneck. Herein, we established an efficient in vitro culture system (termed L15SP) for OSCs derived from Paralichthys olivaceus, consisting of L-15 medium supplemented with15% fetal bovine serum (FBS), 2 μg/L basic fibroblast growth factor (bFGF), 2 μg/L leukemia inhibitory factor (LIF), 50 μmol/L β-mercaptoethanol (β-ME), 1% fish serum, and 18 g/L embryo extract protein, cultured at 23 °C. This system enabled stable long-term passage of P. olivaceus OSCs. Further investigations revealed that interferon-induced transmembrane protein 3 (Ifitm3) was highly expressed on the membrane of P. olivaceus OSCs. Functional assays demonstrated that Ifitm3 significantly enhanced proliferation, migration, and stemness maintenance of long-term cultured OSCs. Ifitm3 positively modulated the expression of key PI3K-AKT signaling components, including pik3cb, pik3r1, and akt2, to regulate downstream OSC functional genes. Upon pathway activation, Ifitm3 facilitated PIP3 enrichment at the OSC plasma membrane, thereby amplifying PI3K-AKT signaling. In conclusion, Ifitm3 governed OSC biological functions by potentiating PI3K-AKT signal transduction. This study establishes a reliable long-term culture system for fish OSCs and identifies a novel functional marker for OSC identification, providing valuable support for fish germplasm preservation and genetic breeding. - Source: PubMed
Publication date: 2026/08/13
Ren YuqinYang YucongWang GuixingHan ZengshengHe NuanWang XiyuanZhang YitongHe ZiyangCui XiaodongHe ZhongweiLiu YufengCao WeiZhang XiaoyanWang YufenKang XianjiangHou Jilun - Resistance to tyrosine kinase inhibitors (TKIs) is a core limitation in the clinical treatment of chronic myeloid leukemia (CML). Although ponatinib can cover the T315I mutation, its clinical application is limited by severe adverse reactions at high doses. On the basis of the USP28-BCR-ABL-IFITM3 resistance signaling axis first identified in our previous study, a ginger-derived lipid carrier-mediated targeted nanodelivery system (IP@GLPs@εF) was constructed, which codelivers CRISPR/Cas9-mediated IFITM3 knockout (IFITM3 KO) plasmid and ponatinib, establishing a new synergistic intervention mode of gene editing and targeted chemotherapy. When modified with ε-polylysine and fucoidan via layer-by-layer self-assembly technology, the carrier has an average particle size of 226.1 nm, a drug encapsulation efficiency of 84.2%, and excellent biocompatibility. experiments confirmed that the optimal ratio (2.5 μg IFITM3-sg3 + 5 μM ponatinib) significantly reversed the drug resistance of K562R cells, promoted apoptosis and inhibited proliferation. experiments using ectopic and orthotopic xenograft models verified that this system can efficiently target tumor tissues and significantly suppress the progression and metastasis of drug-resistant tumors, with no obvious toxic side effects on major organs. Mechanistically, this study revealed that IFITM3 mediates CML resistance by interacting with HSPA9 to activate the MET/AKT/BCL2 pathway and that IFITM3 KO can block this pathway and exert a synergistic antiresistance effect with ponatinib. This research provides a novel IFITM3-targeted synergistic therapeutic strategy and technical support for the clinical treatment of CML resistance. - Source: PubMed
Publication date: 2026/07/28
Feng ZhenyangMa YaofangHu JiahuiWang YanWang KexinYang YingWu QiyuanLou JiatianShi RuoyuanXu KejiaYang WanlinLi LiTu LinglanCheng Liyan