IFNGR2 Antibody
- Known as:
- IFNGR2 Antibody
- Catalog number:
- GWB-MQ504I
- Product Quantity:
- 50ug
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- IFNGR2 Antibody
Related genes to: IFNGR2 Antibody
- Gene:
- IFNGR2 NIH gene
- Name:
- interferon gamma receptor 2
- Previous symbol:
- IFNGT1
- Synonyms:
- AF-1
- Chromosome:
- 21q22.11
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: IFNGR2 Antibody
Related articles to: IFNGR2 Antibody
- Interferon-gamma (IFN-γ) serves as an inflammatory cytokine essential for modulating innate and cell-mediated immune responses by associating with a receptor complex composed of IFNGR1 and IFNGR2. In this research, the entire cDNA of IFNGR2 from Nibea albiflora was cloned and functionally analyzed (referred to as NaIFNGR2), with the complete cDNA sequence measuring 924 bp and encoding 307 amino acids. The phylogenetic analysis and multiple sequence alignment revealed a significant similarity of NaIFNGR2 with homologous sequences found in other bony fish, especially within the FNⅢ domain and the transmembrane region. Real-time PCR analysis revealed that NaIFNGR2 was consistently expressed across all examined tissues, including the head-kidney, spleen, liver, kidney, gill, muscle, and blood, with the highest levels found in the gills. Following stimulation with Polyinosinic-polycytidylic acid (Poly (I:C)), Vibrio alginolyticus, or Vibrio parahaemolyticus, the mRNA levels of NaIFNGR2 showed an increase in a time-dependent manner. Subcellular localization studies indicated that NaIFNGR2 resided on the cell membrane and NaIFN-γ, once synthesized within the cell, was transported to the membrane to interact with NaIFNGR2. Additionally, NaIFNGR1 and NaIFNGR2 were completely co-localized on the cell membrane, which was consistent with the findings that NaIFNGR1 and NaIFNGR2 could form a heterodimeric complex. Being treated with the NaIFN-γ recombinant protein, both alone and in combination with LPS, various concentrations of NaIFN-γ were non-toxic to the growth of RAW 264.7 macrophages and significantly promoted their proliferation. The expression levels of IL-1β, IL-6, and TNF-α proteins were markedly upregulated in a concentration- and time-dependent manner following 24 and 48 h of combined stimulation. Furthermore, the secretion of nitric oxide (NO) was significantly increased after 36 and 48 h of stimulation, highlighting the regulatory effect of NaIFN-γ on macrophages and its influence on the inflammatory response. Collectively, the findings indicated that the NaIFN-γ ligand-receptor system was present in N. albiflora and played a crucial role in the immune response to pathogenic bacterial infections, enhancing our comprehension of the function of IFN-γ within the immunomodulatory processes of teleosts. - Source: PubMed
Publication date: 2026/04/27
Yuan HanbingLiu YongxinZhou XuXu DongdongChi ChangfengLü ZhenmingLiu Huihui - This study aimed to investigate the regulatory role of circular RNAs (circRNAs) in lupus nephritis (LN) and to explore their potential mechanisms. - Source: PubMed
Publication date: 2026/04/24
Gong SiwenWang ChongyaoEmiliia GainetdinovaFu YutingDing XiaotongHe WenyaZhang LeiLiu RuichanWang XingzhiBao YushiSui Manshu - Transient receptor potential (TRP) channels regulate Ca homeostasis and tumor malignant phenotypes, whereas their prognostic relevance and therapeutic implications in glioblastoma (GBM) remain poorly characterized. - Source: PubMed
Publication date: 2026/04/19
Sun RunfengZhu LongLu ZhichaoWang ZihengFeng SuyinZhao Jingwei - Immune checkpoint blockade (ICB) is a standard treatment for several types of human cancer, yet we still lack a deep understanding of the mechanisms underlying primary resistance. Tumor-intrinsic defects in immune recognition and interferon-gamma (IFNγ) signaling pathways facilitate immune evasion and may limit the efficacy of ICB. Here, we delineate the mutational landscape and functional consequences of amino acid substitutions in key immune-related genes, B2M, CALR, IFNGR1, IFNGR2, JAK1, and JAK2, across more than 12,000 primary tumors and cancer cell lines. Genomic alterations affecting the coding regions of at least one of these genes were identified in approximately 11% of cancers, with missense variants accounting for 55% of these events. B2M, encoding the invariant light chain of the heavy chain-I (HLA-I) complex, exhibited the highest mutation frequency per base pair, the mutations predominantly involving truncating variants. A curated set of 2156 missense mutations in B2M and in components of the IFNγ-signaling pathway (IFNGR1, IFNGR2, and JAK2) was analyzed using SIFT, PolyPhen-2, and AlphaMissense, yielding predicted pathogenicity rates of 52%, 35%, and 27%, respectively. The functional assays, performed in lung cancer cells, revealed JAK2 and IFNGR1 variants that impaired IFNγ-mediated transcriptional activation and growth suppression, and B2M variants that disrupted HLA class I complex formation. Notably, AlphaMissense predictions showed the highest concordance with experimental data. These findings provide a detailed mutational map of antigen presentation and IFNγ-response components in cancer. Overall, our results provide a resource of specific mutations in genes involved in immune pathways that compromise tumor immunogenicity and will serve for support in patient selection for response to ICB. - Source: PubMed
Publication date: 2026/04/04
Diaz Cristina AMorillas Juan MNavajas-Chocarro PabloProvenzano ValentinaSetien FernandoEsteller ManelSanchez-Cespedes Montse - Tumor necrosis factor (TNF) orchestrates immune responses but can also drive inflammation-associated tissue damage. However, the mechanisms governing tissue tolerance to TNF remain poorly understood. Here, we reveal that TNF receptor 1 (TNFR1) abundance is regulated by two upstream open reading frames (uORFs) in the 5' untranslated region of and demonstrate that this is a key determinant of TNF tolerance. uORF2 dominantly limits TNFR1 translation, and its disruption increases TNFR1 levels, leading to excessive TNF-induced gene activation and cell death in cell culture. By contrast, uORF1 dynamically regulates TNFR1 levels in response to inflammatory and stress signals. In mice, uORF2 protects against TNF-driven systemic inflammatory response syndrome and liver pathology. We additionally report that the translation of other immune receptor messenger RNAs, including , , and , is also controlled by uORFs. Thus, regulation of TNFR1 levels and possibly of other immune receptors emerges as a mechanism safeguarding against excessive immune responses and tissue damage. - Source: PubMed
Publication date: 2026/04/03
Ma BiaoLyu WenxinRizk JohnHan XiaoyueKjær MajkenPereira Almeida VinnyciusJessen MalinSauerland Max BenjaminLeung Carol Sze KiVan den Eynde Benoit JLu XinGyrd-Hansen Mads