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STAT4Signal Transducer and Activator of Transcription 4
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The rs7574865 and rs10181656 SNPs in the third intron of the STAT4 gene were amplified by polymerase chain reaction (PCR), and the 5'-TTATGGAAAATTACATGAGTGTG-3' and 5'-GCAAATCTTTGTAAAAAGTCAA-3' primers were used to generate a region of 156 bp in the STAT4 gene that could be used in the subsequent genotyping reactions of the rs7574865 polymorphism.
The genotyping of the STAT4 rs7574865 and rs10181656 SNPs was performed using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis.
Analysis of the relationship between the two STAT4 polymorphisms and the clinical and laboratory data of the RA patients.
The genotype distributions and allele frequencies of the STAT4 rs7574865 and rs10181656 polymorphisms were compared between the RA patients and the control group, and the allele frequencies and genotype distributions of all of the analyzed samples of the STAT4 rs7574865 and rs10181656 polymorphisms from both groups are displayed in Table 2 and 3, respectively.
None of the clinical features or disease activity parameters showed any correlation with the rs7574865 and rs10181656 genotype distribution of the STAT4 gene in the RA patients (Table 4a, b).
Specifically, we've found that STAT4 appears to be involved in insulin resistance as well as the development of atherosclerosis," adds Elena V.
Early findings in these studies indicate that insulin resistance and atherosclerosis, a condition characterized by the thickening of artery walls due to fatty plaque deposits, occur in conjunction with elevated levels of STAT4.
The researchers learned that eliminating STAT4 in rodent models reduced the development of atherosclerosis.
Basically," says Jerry Nadler, MD, director of the EVMS Strelitz Diabetes Center, chair of internal medicine and co-author on both papers, "it appears that excess STAT4 is working in hyper-drive, leading to inflamed fat which can produce these problems.
STAT4 encodes a transcription factor that transmits signals induced by several key cytokines, including IL-12 and IL-23, and differentiation of both the Th1 and Th17 proinflammatory T-cell lineages requires STAT4-dependent cytokine signaling.
Two high-density (43,44) and one low-density GWAS45 in SLE have recently been published, yielding definitive data about several new risk genes, as well as valuable confirmatory data related to several previously identified genes, including STAT4 and IRF5.
Overall, the top three genetic loci in their study were the HLA region, and the recently identified STAT4 and IRF5 loci.