Recombinant Human NCR3
- Known as:
- Recombinant Human NCR3
- Catalog number:
- CG15
- Product Quantity:
- 10ug
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Recombinant Human NCR3
Related genes to: Recombinant Human NCR3
- Gene:
- NCR3 NIH gene
- Name:
- natural cytotoxicity triggering receptor 3
- Previous symbol:
- LY117
- Synonyms:
- 1C7, NKp30, CD337
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-05
- Date modifiied:
- 2016-10-05
Related products to: Recombinant Human NCR3
Related articles to: Recombinant Human NCR3
- Epigenetic aging clocks offer precise measures of biological age, yet the causal contributions of immune gene expression within specific cell subtypes to epigenetic aging remain poorly understood. By integrating single-cell eQTL data from the OneK1K cohort with GWAS summary statistics for four epigenetic clocks (HannumAge Acceleration, IEAA, PhenoAge Acceleration, and GrimAge Acceleration), we performed two-sample Mendelian randomization across diverse immune cell subtypes, followed by colocalization analysis and gene-level phenome-wide association studies. We identified 11 eGene-cell type pairs surviving Bonferroni correction, including NUCKS1 in CD4 NC T cells and NCR3 in Classic Monocytes as risk-increasing eGenes for HannumAge Acceleration, and HSPA1B in Classic Monocytes as protective across multiple clocks. ANP32E in Classic Monocytes represented the strongest risk signal for GrimAge Acceleration (OR = 2.683), while BCAS4 in CD8 EM T cells was the strongest protective association (OR = 0.683). Colocalization confirmed NUCKS1 (PP.H4 = 87%) and NCR3 (PP.H4 = 69%) as high-confidence causal eGenes, and PheWAS revealed no genome-wide significant off-target associations for the prioritized targets, supporting their specificity. These findings establish cell subtype-specific causal roles for immune gene expression in epigenetic aging and prioritize NUCKS1, NCR3, and ANP32E as candidate targets for interventions aimed at promoting healthy aging. - Source: PubMed
Publication date: 2026/05/26
Zhang ChunZhang Jingqi - Ovarian cancer exhibits the highest mortality rate among gynecologic malignancies. Platinum resistance remains a key determinant of poor clinical outcomes. Early prediction of platinum resistance is critical for personalized treatment. This study aimed to identify as an independent prognostic biomarker and assess its predictive value for platinum resistance and the tumor immune microenvironment in ovarian cancer. - Source: PubMed
Publication date: 2026/04/28
Qiu MinghuiZhao MengxingZhao JianiZhao HaoyunJiang WeiqiYang LuYang Lindong - Natural killer (NK) cells are effector cells of the innate immune system. The cytokine microenvironment influences NK cell function. Dysregulation of NK cell cytotoxicity can manifest in reproductive disorders and is also observed in tumor-transformed tissues. The search for immunotherapies capable of regulating NK cell activity is therefore relevant. This study aimed to evaluate the effect of the TGFβ signaling pathway inhibitor and the cyclin-dependent kinase (CDK) 7/12/13 inhibitor on the transcriptional profile of NK-92 cell line. In the study, the cytokines TGFβ1, IL-12, IL-15, IL-18, and TNFα, and the TGFβ receptor type 1 (TGFβR1) inhibitor LY3200882 and the CDK7/12/13 inhibitor THZ1 were used. The cells were cultured sequentially in the presence of inhibitors and cytokines, followed by assessment of the gene expression of , , , , , , , , , , and We observed direct effects of the inhibitors on NK cells. LY3200882 increased the expression of and , and reduced . THZ1 increased the expression of , , and , while it reduced and . IL-12, IL-15, IL-18, and TNFα modified the gene expression of some phenotypic and cytotoxic receptors and transcription factors. TGFβ1 increased the expression of , , and . Blocking TGFβ-dependent signaling with LY3200882 abolished TGFβ1 effects. We assessed CD56 presence on NK-92 cell membrane and found its increase in the presence of LY3200882. After LY3200882 treatment, in the presence of TGFβ1 and choriocarcinoma cell line JEG-3, the expression of CD56 receptor on NK cell membrane decreased. Pretreating NK cells with THZ1 decreased the expression of , , and in the presence of TGFβ1. Thus, LY3200882 partially neutralized TGFβ1 effects on the expression of NK cell receptor genes. THZ1 followed by TGFβ1 treatment promoted NK cell transcriptional profile characteristic for CD56dim NK cells. Both LY3200882 and THZ1 affected the NK cell transcription even without cytokine treatment. The independent effects of synthetic inhibitors on NK cells, as well as their influence in the presence of tumor cells, should be considered. - Source: PubMed
Publication date: 2026/04/17
Mikhailova ValentinaMarko OksanaMkrtchyan EdgarSokolov Dmitry - Epstein-Barr virus (EBV) is a human γ-herpesvirus that establishes latency and lifelong infection in B cells. Failure to control latent EBV infection can result in a variety of malignancies, including lymphoproliferative diseases. Studies have implicated natural killer (NK) cells as critical in the host defense against lytic and latent EBV infection. To fully characterize NK cells that respond to latently infected cells, we generated a panel of EBV+ B lymphoblastoid cell lines (EBV+ LCL) and performed coculture experiments with autologous primary NK cells. EBV-responsive NK cells were analyzed for functional and phenotypic markers using mass cytometry. In addition to expression of the inhibitory NK cell receptor NKG2A, EBV-responsive NK cells express high levels of the NKp30 and NKG2D activating receptors which were shown to be important in mediating cytotoxicity of EBV+ LCL. NK cells from cohorts of EBV seropositive and EBV seronegative children were examined by mass cytometry for NK cell receptor expression and identified 4 NKG2A+ clusters, including the NKG2A+2B4+CD56+CD16-CD57-NKG2C-NKp30+NKG2D+ population. The importance of the NKG2A: HLA-E immune checkpoint axis was established using both HLA-E knockout EBV+ LCL and antibody blockade of NKG2A which demonstrated enhanced NK-mediated cytotoxicity in the absence of NKG2A-HLA-E interactions. Taken together, our results support that NKG2A+ NK cells are educated and functionally cytotoxic against EBV-infected B cells and suggest therapeutics targeting the NKG2A: HLA-E immune checkpoint axis would be a good option for EBV-associated malignancies. - Source: PubMed
Pena Josselyn KZhang WenmingBadshah Joshua SLedezma-Soto CeciliaJenkins Kayla CToh JiayingKirchner Varvara AEsquivel Carlos OMartinez Olivia MKrams Sheri M - Synthetic multimeric peptide ligands of the natural cytotoxicity receptor, NKp30, on natural killer cells were developed in this study. A divergent solid phase peptide synthesis strategy was optimized for the conjugation of multiple peptide ligands, based on the parent TVPLN and related permutation sequences, into branched and hyperbranched peptides for structure-activity relationship studies. According to CD spectroscopy in aqueous trifluoroethanol, the parent TVPLN peptide transitioned from a β-turn (monomer and dimer) to an extended β-sheet and a helix-type conformation in its branched (trimer) and hyperbranched (tetramer) structures. The multimeric peptides were predicted to expand the binding interface to NKp30 according to molecular modeling and docking predictions. Flow cytometry revealed greater binding activity of the trimer and tetramer ligands onto NKp30-coated beads and the natural killer cells, while being displaced by the native B7H6 ligand in competitive binding studies on the NKp30-coated beads and reducing anti-NKp30 binding on the natural killer cells, suggesting some receptor-specific binding activity. Immunostimulatory activity assays showed little secretion of TNF-α and IFN-γ from the natural killer cells following peptide treatment, with the TVPLN monomer and dimer remaining superior to the rest. Select changes in sequence compositions and the ligated multimeric peptide display had an inhibitory effect on natural killer cell activation. This result was likely due to changes in bound vs unbound multimeric peptide structures that deviated from the bioactive β-turn of the TVPLN monomer and dimer for direct peptide engagement at the NKp30 active site. Nonetheless, the novel multimeric peptides showed improved cell binding activity relative to their linear counterparts and were nontoxic at lower (10 μM) doses, making them safe and effective for structure-activity studies for the discovery of novel peptide ligands of natural killer cells. - Source: PubMed
Publication date: 2026/01/19
Allen Mitchell CCollak Filiz KDaniel GraceLeblanc MeghanKurdieh ReemArdolino MicheleBiggar Kyle KSabatino David