Karen M. Kroeger

TL;DR: It is demonstrated that the region (−323 to −285) encompassing −308 in the TNF2 allele binds nuclear factors differently to the same region in the promoter of the more common TNF1 allele, suggesting that the −308 GA polymorphism may play a role in the altered TNF-α gene expression observed in individuals with the HLA Al, B8, DR3 haplotype.

TL;DR: The majority of the data support a direct role for the T NF2 ‐308 allele in the elevated TNF levels observed in TNF2 homozygotes and HLA‐A1, B8, DR3 individuals.

TL;DR: This study supports the usefulness of BRET as a powerful tool for studying GPCR aggregations and receptor/protein interactions in general and presents evidence that the functioning unit of TRHRs exists as homomeric complexes.

TL;DR: It was found that a difference in TNF1 and TNF2 promoter activities was only observed in U937 and Jurkat cells, and not in Raji (B cell line), HeLa (epithelial carcinomacell line), HepG2 (hepatoma cell line) or THP-1 (monocyte), suggesting cell-type specific transcription factors or modifications may be involved in the formation of the -308 protein/DNA complex.

TL;DR: It is concluded that glucocorticoid drugs suppress LPS-stimulated secretion of TNF-α from human monocytic cells largely through antagonizing transactivation by c-Jun/ATF-2 and NF-κB complexes at binding sites in the −106 to −88 bp region of the T NF-α promoter.