Rabbit Anti-Human STAT4 Polyclonal Antibody Knockout Validated

The signal transducer and activator of transcription 4 (STAT4) gene encodes a transcription factor that transmits signals induced by several cytokines which play critical roles in the development of autoimmune and chronic inflammatory diseases. We performed an association study between STAT4 single nucleotide polymorphisms (SNPs) and tuberculosis (TB). 624 TB cases and 598 healthy controls were studied to compare allele/genotype frequencies of 4 SNPs in STAT4. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using logistic regression. Genotyping was performed with the Sequenom MassARRAY SNP genotyping platform. Out of 4 SNPs tested in the study, rs4853542 allele A showed a 25% decreased risk of TB compared with allele G (P = 0.013, OR = 0.75, 95%CI: 0.60-0.94). However, it did not show significant differences under any genetic model after Bonferroni correction. No association was found for the other 3 SNPs with TB. In subgroup analyses, the protective effects of rs485342 allele A were stronger among younger subjects < 25 years (P = 0.002, OR = 0.49, 95%CI: 0.31-0.76). Allele A of the rs4853542 polymorphism in STAT4 is not associated with TB susceptibility, but we demonstrated that rs4853542A allele decreased risk of TB in younger adults after Bonferroni correction.

Rheumatoid arthritis is an autoimmune disease that affects several organs and tissues, predominantly the synovial joints. The pathogenesis of this disease is not completely understood, which maybe involved in the genomic variations, gene expression, protein translation and post-translational modifications. These system variations in genomics, transcriptomics and proteomics are dynamic in nature and their crosstalk is overwhelmingly complex, thus analyzing them separately may not be very informative. However, various '-omics' techniques developed in recent years have opened up new possibilities for clarifying disease pathways and thereby facilitating early diagnosis and specific therapies. This review examines how recent advances in the fields of genomics, transcriptomics and proteomics have contributed to our understanding of rheumatoid arthritis.