IndraLab

"Tumor necrosis factor (TNF) alpha induced FLAP mRNA expression, FLAP promoter activity, and C/EBP alpha, delta, and epsilon binding to the proximal and distal promoter consensus sites."

"IAP, inhibitor of apoptosis; SMAC, second mitochondria-derived activator of caspase. In the death receptor pathway, ligands such as tumour-necrosis factor (TNF), FAS ligand (also known as CD95L), or TNF-related apoptosis-inducing ligand (TRAIL, also known as APO2 ligand (APO2L) or TNF ligand superfamily member 10 (TNFSF10)) interact with their respective death receptors (TNF receptor 1 (TNFR1), FAS (also known as CD95) and death receptor 4 (DR4, also known as TRAIL receptor 1 (TRAILR1)) or DR5 (also known as TRAILR2), respectively). These interactions ultimately lead to the recruitment of the FAS-associated death domain (FADD) and the activation of the protease caspase 8. Caspase 8 cleaves and activates caspase 3 and other downstream caspases, which results in a proteolytic cascade that gives rise to the cell death phenotype characterized by DNA fragmentation, chromatin condensation, cell shrinkage and membrane blebbing."

"Overexpression of NCOA-1, NCOA-2, and NCOA-3 enhanced E2-mediated gene expression by 3.17 +/- 0.51-, 2.33 +/- 0.8-, and 3.65 +/- 0.65-fold, respectively, and enhanced cell survival by suppressing tumor necrosis factor alpha (TNF-alpha)-induced cell death Overexpression of NCOA-1 and NCOA-3 exerted potent survival effects in breast carcinoma cells."

"In contrast, the expression of cyclin D and E and the phosphorylation of Rb protein were not affected by ectopic expression of the drs gene, suggesting that an Rb-independent downregulation of cyclin A is involved in the suppression of anchorage-independent growth by means of the drs gene."