Anti-FASL polyclonal antibody [Biotin]

FAS rs2234767 (-1377 G>A), rs1800682 (-670 A>G) and FASLG rs763110 (-844 C>T) promoter polymorphisms can influence transcriptional activities of the genes and thus multiple tumors susceptibility. To investigate their association with risk of colorectal cancer (CRC), the three SNPs were genotyped in 878 cases and 884 controls and the results showed that the FAS rs2234767 and rs1800682 were in a high linkage disequilibrium (LD) with each other (D' = 0.994) and jointly contributed to an increased risk of CRC (without vs. with rs2234767 GG/rs1800682 AA genotypes, adjusted OR = 1.30, 95% CI = 1.05 - 1.61). In vivo ChIP assays evaluated the effect of rs2234767 and rs1800682 on recruitment of SP1 and STAT1, respectively, to chromatin. The results showed SP1 interacting specifically with STAT1 recruited to their respective motifs for transcriptional activation. The mutant alleles rs2234767 A and rs1800682 G jointly affected coupled SP1 and STAT1 recruitment to chromatin. The interplay between SP1 and STAT1 was critical for the functional outcome of rs2234767 and rs1800682 in view of their high LD. In conclusion, the FAS rs2234767 and rs1800682 polymorphisms were in high LD with each other, and they jointly contributed to an increased risk of CRC by altering recruitment of SP1/STAT1 complex to the FAS promoter for transcriptional activation.

OBJECTIVE: This study aimed to explore the molecular mechanism of osteoarthritis (OA) development and discover underlying genes associated with OA. DATA AND METHODS: Gene expression profile GSE48556 including 106 peripheral blood mononuclear cells (PBMCs) of osteoarthritis patients and 33 PBMCs of healthy controls was downloaded from the Gene Expression Omnibus database. The limma package was used to identify the differentially expressed genes (DEGs) by paired t-test. The functional enrichment analyses of DEGs was performed, followed by the construction of protein-protein interaction (PPI) network. RESULTS: Total 432 DEGs including 178 up-regulated DEGs and 254 down-regulated DEGs were identified. Pathways of cytokine-cytokine receptor interaction and T cell receptor signaling pathway were significantly up-regulated in OA. Biological processes of negative regulation of transcription from RNA polymerase II promoter and negative regulation of transcription, DNA-dependent were significantly down-regulated in OA. The platelet-derived growth factor receptor, beta polypeptide (PDGFRB), interferon, gamma (IFNG), early growth response 1 (EGR1), Fas ligand (TNF superfamily, member 6) (FASLG), H3 histone, family 3B (H3.3B) (H3F3B) and so on had higher connectivity degree in the PPI networks. CONCLUSIONS: DEGs of OA were mainly enriched in the pathways associated with cytokine-cytokine receptor interaction and T cell receptor signaling pathway. The DEGs such as PDGFRB, IFNG, EGR1, FASLG and H3F3B may be the potential targets for OA diagnosis and treatment.