Human TNFRSF6B (Tumor necrosis factor receptor superfamily member 6B) ELISA Kit

Familial clustering and genome-wide linkage scans strongly support a genetic susceptibility to familial IgA nephropathy(IgAN), but genetic factors that predispose to sporadic IgAN are unknown. A high-throughput single nucleotide polymorphism (SNP) association study was conducted using a customized Illumina BeadChip in 732 white patients with biopsy-proven IgAN and 503 control subjects from Canada, France, and Finland. Approximately 93% of 1536 SNPs on the array were tag SNPs from Phase I+II of the HapMap with a minor allele frequency >= 5%, designed to capture the common variants of genes within the critical interval of IGAN1 on chromosome 6q22 and 69 biologic candidate genes for IgAN. SNPs of suggestive or significant association were identified by using logistic regression to adjust for age, gender, study site, and population stratification. Despite using a dense marker set that covered an average interval of 6.5 kb between SNPs, there was no strong and consistent association signal within the IGAN1 critical interval. Among the biologic candidate genes examined, two significant association signals were found at IL5RA and TNFRSF6B, the latter being particularly interesting because this gene encodes a decoy receptor for a TNF family ligand that causes IgAN in mice when overexpressed. Pending replication, these data suggest that variants of IL5RA and TNFRSF6B may predispose to sporadic IgAN.

The tumor necrosis factor receptor super-family member 6b (TNFRSF6B) is over-expressed in various human cancers, but its function in hepatocellular carcinoma (HCC) remains uncertain. The aim of the study was to investigate the relationship between TNFRSF6B expression and apoptosis in HCC and the effect of anti-TNFRSF6B neutralization monoclonal antibody (McAb) on HCC cells. TNFRSF6B mRNA and protein expression were compared with apoptosis in 78 cases of HCC. Proliferation, cell cycle, apoptosis, and migration ability of liver cancer cells co-cultured with anti-TNFRSF6B McAb were also detected. TNFRSF6B mRNA and protein expression in the tumor tissues negatively correlated with apoptosis. Cell proliferation was decreased, cell cycle was arrested in G1/S-phase, apoptosis was increased, and migration ability was inhibited by anti-TNFRSF6B McAb in vitro. Anti-TNFRSF6B McAb could be useful to suppress proliferation and induce apoptosis in HCC. Thus, TNFRSF6B might be a critical, targeted therapy strategy for HCC. (C) 2010 Elsevier GmbH. All rights reserved.