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
- 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 - The biogenesis of integral membrane proteins is complex, as revealed by an ever-growing number of cellular components dedicated to the insertion, folding, surveillance, rectification, or quality control of specific client membrane proteins. The zinc metalloprotease ZMPSTE24 and its yeast homolog Ste24 have well-established roles in the proteolytic maturation of the nuclear scaffold protein lamin A and yeast a-factor, respectively. Additionally, Ste24 has been implicated through yeast genetic screens in a variety of membrane processes, including ER- associated degradation (ERAD), Sec61 translocon "unclogging," and potentially as a membrane protein topology determinant. Recently, an interaction was demonstrated between ZMPSTE24 and the antiviral interferon induced transmembrane protein IFITM3, although the functional significance of this interaction is poorly understood. IFITM3 is a tail-anchored protein with a cytoplasmic N-terminus, a single transmembrane span, and a lumenal/exocellular C-terminus. Here, we show that a catalytic-dead version of ZMPSTE24, ZMPSTE24, exhibits enhanced binding to IFITM3, and this bound species of IFITM3 is hypo-palmitoylated. Using a split fluorescence topology reporter, we demonstrate that ZMPSTE24 "traps" and stabilizes a subpopulation of IFITM3 molecules with an atypical membrane topology, whose C-terminus is cytosolic instead of lumenal. Such inverted forms of IFITM3 are also detected in the presence of ERAD inhibitors or for a lysineless version of IFITM3. We hypothesize the ZMPSTE24 trap mutant reveals a normally transient isoform of IFITM3 whose transmembrane span is inverted and that ZMPSTE24 is involved in the quality control of IFITM3 topology, either inverting, correcting or assisting in removal of aberrant IFITM3 molecules. - Source: PubMed
Publication date: 2026/08/11
Spear Eric DShilagardi KhurtsSarju SoniaMichaelis Susan - Cerebral ischemic stroke triggers extensive neuronal membrane breakdown, releasing a massive load of cholesterol that overwhelms resident microglia. Dysregulated microglial cholesterol metabolism has been implicated in post-stroke neuroinflammation, yet the specific pathogenic microglial subpopulations, their molecular signatures, and the downstream inflammatory cascades remain poorly defined. - Source: PubMed
Cheng YueZhou YuxiChen YonghuiShen TianniLi YanChen ChenFan QiuyueQi JieLi PeiyingZhang Yueman - Intrinsic innate immune barriers have evolved to suppress viral infection and can reduce effective gene delivery in gene therapy. We have developed BG147, a novel cyclosporine A (CsA) analogue optimised via structure-guided design to specifically inhibit interferon-induced transmembrane proteins (IFITM1-3) but not inhibit CsA target, and HIV cofactor, cyclophilin A. BG147 enhances VSV-G pseudotyped lentiviral vector transduction ex vivo in hematopoietic stem and progenitor cells (HSPCs) and in in vivo ocular gene therapy of photoreceptor cells in mice. Upon BG147 treatment, IFITM3 protein is mislocalised and degraded through lysosomal acidification-dependent pathways but returns 96 h after BG147 washout. Critically, HSPC transduced in the presence of BG147 showed successful engraftment in NGS mice. BG147 promises to transform ex vivo and in vivo gene therapies by transiently inhibiting intrinsic immune barriers mediated by IFITM3 to enhance a wide range of protocols. - Source: PubMed
Publication date: 2026/08/03
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