Rabbit Anti-Human IFNGR1 (Phospho Tyr457) Polyclonal antibody

Ifng/Ifngr1 are the main genes that are associated with tuberculosis. We continued to search for other functional single nucleotide polymorphisms (SNP) and investigated their influence on patients with tuberculosis in the Chinese population. Seven SNP located in the ifng and ifngr1 genes were genotyped by ligase detection reaction in 222 cases and 188 ethnically matched controls. A significant genetic association between rs7749390 (located on the exon/intron splice site of the ifngr1 gene) and tuberculosis was observed, and the log-additive model was accepted as the best inheritance model to fit these data (OR: 1.35, 95% CI: 1.02-1.80, P = 0.038). Haplotype-specific association analysis revealed that the result was consistent with the individual SNP study. The combination of rs2234711/rs1327474/rs7749390/rs41401746, which was in strong linkage disequilibrium (D' > 0.75), showed a significant association of ifngr1 with tuberculosis (P = 0.00079). Neither the single SNP nor the haplotype analysis showed a significant association between tuberculosis and the ifng gene markers. Our data implied the involvement of the ifngr1 gene in susceptibility to tuberculosis.

Although small-molecule targeting of EZH2 appears to be effective in lymphomas carrying EZH2 activating mutations, finding similar approaches to target EZH2-overexpressing epithelial tumors remains challenging. In MYC-driven, but not PI3K-driven prostate cancer, we show that interferon-gamma receptor 1 (IFNGR1) is directly repressed by EZH2 in a MYC-dependent manner and is downregulated in a subset of metastatic prostate cancers. EZH2 knockdown restored the expression of IFNGR1 and, when combined with IFN-gamma treatment, led to strong activation of IFN-JAK-STAT1 tumor-suppressor signaling and robust apoptosis. Pharmacologic depletion of EZH2 by the histone-methylation inhibitor DZNep mimicked the effects of EZH2 knockdown on IFNGR1 induction and delivered a remarkable synergistic antitumor effect with IFN-gamma. In contrast, although they efficiently depleted histone Lysine 27 trimethylation, EZH2 catalytic inhibitors failed to mimic EZH2 depletion. Thus, EZH2-inactivated IFN signaling may represent a therapeutic target, and patients with advanced prostate cancer driven by MYC may benefit from the combination of EZH2 and IFN-gamma-targeted therapy.