Ask about this productRelated genes to: IFNa2 protein (Mouse)
- Gene:
- IFNA2 NIH gene
- Name:
- interferon alpha 2
- Previous symbol:
- -
- Synonyms:
- IFNA, IFN-alphaA
- Chromosome:
- 9p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-01-14
- Date modifiied:
- 2016-10-05
Related products to: IFNa2 protein (Mouse)
Related articles to: IFNa2 protein (Mouse)
- Cow's milk allergy (CMA) is one of the most common food allergies in childhood frequently associated with body growth impairment and micronutrient deficiencies. Immunonutrition approach with selected bioactive compounds may have beneficial effects on nutritional status and immune tolerance mechanisms. We evaluated the effects of an immunonutrition approach, based on the use of a novel multicomponent food supplement containing prebiotics, postbiotics, vitamin D3, docosahexaenoic acid (DHA), extracts, and Quercetin in children with CMA. - Source: PubMed
Publication date: 2026/03/16
Carucci LauraCaldaria ErikaOglio FrancaIorio Raffaele FedericoMauriello VittoriaMasino AntonioCoppola Serena - Prediabetes is accompanied by early β-cell stress and oxidative imbalance before overt hyperglycemia. Circulating extracellular vesicle (EV) microRNAs (miRNAs) may capture early metabolic disturbances, but their mechanistic relevance remains unclear. Plasma EV miRNA profiles were analyzed across normoglycemia, prediabetes, and newly diagnosed type 2 diabetes, with validation in an independent cohort (n = 150). Functional studies were performed in pancreatic β-cells exposed to glucolipotoxic stress to examine miRNA regulation, IFN-α signaling, mitochondrial redox status, and insulin secretion. Six EV miRNAs, including miR-186-5p, were consistently reduced in prediabetes and correlated with glycemic and insulin resistance indices. In β-cells, glucolipotoxic stress selectively suppressed miR-186-5p, leading to derepression of IFNA2, activation of IFN-α-JAK/STAT signaling, increased mitochondrial ROS, impaired ATP/ADP dynamics, and reduced glucose-stimulated insulin secretion. Restoration of miR-186-5p or pharmacologic JAK inhibition mitigated these defects, and luciferase assays confirmed IFNA2 as a direct target of miR-186-5p. EV-associated miR-186-5p represents an early marker of metabolic stress in prediabetes and provides mechanistic insight into IFN-α-driven oxidative and secretory dysfunction in β-cells. - Source: PubMed
Publication date: 2026/01/23
Park Jae-HyungNguyen Thi NhiShim Hye MinBae Yun-UiYu Gyeong ImKang JunhoHa Eun YeongCho Hochan - Alphainterferons are cytokines that became famous in the treatment of certain infections and tumors due to their antiviral, antiproliferative, and immunomodulatory activities. While the production of these small proteins in Escherichia coli is well established, high-level overexpression typically results in the formation of insoluble and inactive inclusion bodies that need to be processed through costly and lengthy steps. Here we describe an optimized, inducer-free expression system using E. coli BL21 (DE3) and a pET-based vector with the human IFN-α2a gene. By strategically transitioning the culture from high-temperature biomass accumulation (37 °C) to mild conditions (16 °C) during the early-midlog phase, we leveraged basal expression to favor folding over aggregation. This approach achieved a cytoplasmic solubility of up to 75 %. The protein was recovered using a streamlined one- or two-step ion-exchange chromatography protocol, resulting in maximum purified yields of 23.5 mg/L. Characterization tests confirmed the protein's identity, high purity, in vitro activity, and correct disulfide bonding pattern. This method provides a cost-effective alternative for the production of soluble alphainterferon by eliminating the need for chemical inducers and complex refolding processes. - Source: PubMed
Publication date: 2026/01/28
Bretas Rodrigo MartinsAlves da Silva Marcus ViníciusLeclercq Sophie YvetteGómez-Mendoza Diana Paolada Silva Cunha ArmandoSilva Lopes Luciana Maria - Screening soluble protein ligands is essential for understanding signaling interactions and enabling drug discovery. Currently, screens require arrayed formats because ligand diffusibility causes non-cell-autonomous effects. To enable multiplexed pooled assaying, we developed Obligate Autocrine Signaling In situ Screening (OASIS). Using lentiviral delivery of genetically barcoded ligands fused to a tethering domain, we anchor proteins to the expressing cell's outer membrane, exclusively enforcing autocrine signaling. Validation using IFNA2 and EGF demonstrated uncompromised autocrine signaling with significantly reduced paracrine activity. We leveraged OASIS to perform a pan-ligandome fitness screen of all 770 validated human ligands in KOLF2.1J hiPSCs, identifying potent self-renewal factors, including FGF family ligands, which we experimentally validated in soluble form. Finally, we performed single-cell Perturb-Seq to map the transcriptional remodeling induced by the pan-ligandome library. OASIS provides a generalizable framework to accelerate functional interrogation of the human ligandome and novel peptide binders within live cells and diverse lineages. - Source: PubMed
Publication date: 2025/12/23
Lee Yi-HungDoctor YeshZhang YifanKumar SatheeshRainaldi JosephPan EmilyMali Prashant - The yak, a livestock breed native to Qinghai Province in China. However, the low intramuscular fat (IMF) content of yak meat negatively impacts its taste and flavor, reducing its relative economic value. The experiment was conducted by inhibiting the expression of miR-127 and miR-375 in yak precursor adipocytes. To explore its effect on the proliferation and differentiation of yak adipocyte precursors, and then analyze the molecular regulatory mechanisms of miR-127 and miR-375 on IMF deposition in yak. Furthermore, using RNA-Seq analysis, this study identified the differentially expressed genes (DEGs) and functional pathways regulated by miR-127 and miR-375 that influence IMF deposition. Cellular functional validation experiments showed that inhibiting miR-127 can suppress the proliferation of yak intramuscular preadipocytes and promote their differentiation. Meanwhile, the inhibition of miR-375 had the opposite effect, promoting proliferation and inhibiting differentiation. RNA-Seq analysis revealed that miR-127 inhibition altered the expression of several DEGs, including IFNB1, IFNA2, FABP4, CCL5, ITPKA, and IP6K3. Similarly, the inhibition of miR-375 affected the expression of genes such as IFNB1, IFNA2, FABP4, CCL5, FOS, and IL6. Functional enrichment analysis revealed that many of these DEGs were involved in key signaling pathways, such as the Phosphatidylinositol 3-Kinase-Protein Kinase B (PI3K-Akt) signaling pathway, the Mitogen-Activated Protein Kinase (MAPK) signaling pathway, and the Toll-like receptor (TLR) signaling pathway. Of these, the TLR signaling pathway showed the most significant enrichment of DEGs. Notably, IFNB1, IFNA2, and IL6 appeared to regulate the proliferation and differentiation of intramuscular preadipocytes in yaks by activating the TLR signaling pathway, thereby influencing IMF deposition. - Source: PubMed
Publication date: 2025/12/12
Su QuyangangmaoGui LinshengWu ZhenlingJi QiurongZhu KainaHe TingliChen XuanLiu Guiyao