IL-15 Recombinant Protein
- Known as:
- Interleukin-15 Recombinant Protein
- Catalog number:
- ZR-40-476
- Product Quantity:
- 0.002 mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- IL-15 Recombinant Protein
Related genes to: IL-15 Recombinant Protein
- Gene:
- IL2RB NIH gene
- Name:
- interleukin 2 receptor subunit beta
- Previous symbol:
- IL15RB
- Synonyms:
- CD122
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-01-22
- Date modifiied:
- 2016-10-11
- Gene:
- IL15 NIH gene
- Name:
- interleukin 15
- Previous symbol:
- -
- Synonyms:
- IL-15, MGC9721
- Chromosome:
- 4q31.21
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-11
- Date modifiied:
- 2016-10-05
Related products to: IL-15 Recombinant Protein
Related articles to: IL-15 Recombinant Protein
- Triple-negative breast cancer (TNBC) is among the most life-threatening women malignancies with largely uncharacterized pathogenic mechanisms. While N6-methyladenosine (m6A) methylation has been documented to impact carcinogenesis through extensively altering the gene expression profile, its precise role in TNBC remains poorly understood. Here, we found that insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) promotes TNBC progression in an m6A modification-dependent way. Mechanistically, IGF2BP3 binds to and stabilizes the mRNA of a transcription factor, HOXB9, which subsequently licenses the expression of interleukin 15 receptor α subunit (IL-15RA). The IL-15/IL15RA signaling thus potentiates the migration and invasion of neoplastic cells and contributes to in vivo metastasis of TNBC. These observations provide novel insights into the role of RNA modification in the occurrence of TNBC, and demonstrate the applicability of targeting the m6A machinery especially specific reader proteins in the clinical treatment of advanced TNBC. - Source: PubMed
Publication date: 2026/05/22
Zhang XinhaoWang YehaoWang NaWang TingJiang Tongtong - Interleukin-15 (IL-15) is expressed in various cancers, including melanoma, where it exists in distinct membrane-associated isoforms. Primary melanoma cells predominantly express the non-cleavable transmembrane form (tmbIL-15), while metastatic cells also express a cleavable membrane-bound form (mbIL-15) complexed with IL-15Rα. As tmbIL-15 is capable of reverse signaling upon IL-15Rα engagement, we investigated how this signaling axis modulates melanoma cell behavior across tumor stages. Transcriptomic analysis of melanoma patients revealed that high IL-15 expression correlates with immune activation, inflammation and epithelial-to-mesenchymal transition (EMT), along with coordinated upregulation of IL-15 receptor subunits. Proteomic profiling of melanoma cell lines stimulated with soluble IL-15Rα (sIL-15Rα) uncovered distinct, stage-specific responses. Although several proteins were commonly deregulated across cell lines, most showed opposite regulation in primary versus metastatic models, indicating that tmbIL-15 reverse signaling triggers context-dependent programs influenced by tumor progression. A stringent cross-comparison identified five proteins (PSAP, MARCKS, eEF1A1, DDX39B, and RACK1) as consistently and differentially regulated across tumor stages. Further comparison with published NK cell co-culture and EMT cytokine stimulation datasets revealed a subset of shared effectors, notably PSAP, TPM3 isoform 2 and MARCKS, suggesting that IL-15Rα-induced tmbIL-15 signaling is part of the immune editing phenomenon eliciting pro-tumoral activities complementary to the EMT process. Among these, PSAP emerged as the most robustly and consistently modulated effector, upregulated in primary melanoma cells and downregulated in metastatic ones upon sIL-15Rα stimulation. Its expression correlated positively with CD8+ T cell infiltration and negatively with NK cell infiltration, with distinct transcriptomic programs associated with high PSAP expression in primary versus metastatic settings. Altogether, these findings identify PSAP as a stage-specific mediator of tmbIL-15 reverse signaling in melanoma, integrating immune and EMT-related cues with potential implications for tumor progression and microenvironmental remodeling. - Source: PubMed
Publication date: 2026/04/15
Forcelloni SergioGiron-Michel JulienDel Boccio PieroCufaro Maria ConcettaDi Sebastiano AliceMariotti Francesca RomanaCiancaglini CeciliaChouaib SalemPadelli MaelVespa SimoneMac Giang DangEbert StefanBuart StéphanieMaggi EnricoMoretta LorenzoVacca PaolaTumino NicolaQuatrini LindaCaruana IgnazioAzzarone BrunoSantopolo Silvia - Major Depressive Disorder (MDD) is a serious mental illness, and neuroinflammation is increasingly recognized as a contributor to its pathogenesis; however, the underlying cellular and molecular mechanisms remain largely unknown. In this study, we performed single-nucleus RNA sequencing to profile prefrontal cortex transcriptomics in interleukin-15 receptor subunit alpha knockout (Il15ra) mice displaying depressive-like behaviors. Il15ra mice exhibited cell-type-specific transcriptomic alterations, particularly affecting synapse assembly. Co-expression network analysis identified two gene clusters predominantly linked to synaptic pathways in microglia, excitatory neurons, and interneurons, suggesting dysregulated neuron-microglial interactions in depression. Morphological analysis revealed microglial activation and synapse remodeling driven by enhanced neuron-microglia communication via the CX3CL1/CX3CR1 signaling pathway. Pharmacological inhibition of CX3CL1/CX3CR1 signaling using a CX3CR1 antagonist reversed depressive-like behaviors and microglia-mediated excessive synapse pruning caused by IL-15RA deficiency. Collectively, these findings demonstrate that IL-15RA deficiency contributes to depression onset by modulating microglia-mediated synaptic remodeling, highlighting a targetable neuroimmune pathway for therapeutic interventions in MDD. - Source: PubMed
Publication date: 2026/04/22
Tang YueHuang YuPan JingLi ChaolanYang JieTan XunminHu KanganWen LuXie PeijunLiu YuxiangXu HaotianCao ShixinZhang JianpingLi YifanLiu PingYuan MinghaoSong XiaodongWu JingHe YiWong Ma-LiLicinio JulioZheng Peng - Excessive macrophage activation is thought to be the primary cause of the cytokine storm that results in severe coronavirus disease 2019 (COVID-19) complications. The underlying mechanisms remain elusive, and more research is needed to find disease-critical genes and develop effective therapies. In this study, we used publicly accessible microarray datasets of cytokine storm in cultured human monocyte-derived macrophages challenged with cytokines, and employed bioinformatics, such as weighted gene co-expression network analysis (WGCNA) and differential expression analysis, to dissect gene expression profiles and identify putative disease-related molecules. Initially, three co-expression modules and related key genes were discovered, which highly correlated to macrophages challenged with cytokines. Then, a preliminary gene expression signature consisting of 203 upregulated and 24 downregulated genes was identified. Next, protein-protein interaction analysis and hub gene identification were used to identify 11 crucial hub genes, namely (), (), (), (), (), (), (), (), (), () and (). Then, the LINCS L1000 characteristic direction signatures search engine (L1000CDS2) was employed for drug repurposing studies. Dasatinib was predicted to be the leading therapeutic compound to perturb the gene signature of cytokine storm in human macrophages. Connectivity Map results suggested that dasatinib may normalize ICAM-1 expression. In addition, the results of molecular docking studies and molecular dynamics simulation revealed that dasatinib may spontaneously interact with ICAM-1 via several key residues and form a relatively stable protein-ligand complex. Overall, this work, based on an analysis of co-expression correlation networks, gene expression signatures and pivotal genes in human macrophages challenged with cytokines, combined with drug repurposing studies, demonstrated that dasatinib may interact with ICAM-1 and could be a potential candidate for cytokine storm. However, due to the limitations of computational approaches, further experimental validation is necessary. - Source: PubMed
Publication date: 2026/03/27
Chen ShaojunWu DapengZheng ZheLuo YiyuanZhang Lihua - Viral reservoir presents a significant challenge in HIV-1 cure. We previously observed that Thymosin α1 (Tα1) may restrict the reservoir through the IL-15 pathway. However, the precise mechanism remains to be fully elucidated. Peripheral blood mononuclear cells (PBMCs) were obtained from people living with HIV-1 (PLWH). In vitro, THP-1 cells were differentiated into mature monocyte-derived dendritic cells (MoDCs) and co-cultured with PBMCs under various conditions. Intracellular HIV-1 p24 levels, CD8+ T and NK cell functionality, and reservoir size were evaluated. In vitro, Tα1 stimulation of MoDCs resulted in significant immune response and secretion of IL-15/RA complex ( < 0.001). This interaction with IL-2 Rβ/γ receptors on T cells enhanced the intracellular secretion of CCL3/5, IFN-γ, and TNF-α in CD8+ T cells ( < 0.05), which inhibited p24 levels in CD4+ T cells ( = 0.002), and reduced HIV-1 integrated DNA levels ( = 0.012). Furthermore, the secretion levels of IFN-γ, TNF-α, and GZMB in NK cells and proportion of CD8+ T cells significantly increased following co-culture. These alterations were found to be markedly inversely associated with reservoir size and reactivation. However, these effects were observed in PBMCs from immunological responders (CD4+ T cell count > 350 cells/µL) rather than nonresponders. Tα1 enhances CD8+ T cell function, promotes T proliferation, and suppresses reservoir size and reactivation via IL-15 pathway activation in dendritic cells, which warrants testing in functional cure trials in the future. - Source: PubMed
Publication date: 2026/03/23
Chen ChaoyuXun JingnaWang JiangrongZhang RenfangQi TangkaiLiu LiZhang XinyuSong ZichenShen YinzhongLu HongzhouChen Jun