TNFalpha/CHX treatment led to increased phosphorylation of p38 MAPK and rapid degradation of eIF4E regulator, 4E-BP1, in a p38 MAPK-dependent manner. We show that CHX decreases the expression and activity of PP2A, a phosphatase known to dephosphorylate both p38 MAPK and 4E-BP1. Furthermore,...
In this thesis, we report that induction of apoptosis in human umbilical vein endothelial cells (HUVECs) by treating them with a combination of TNFα and cycloheximide (CHX) [TNFα/CHX] led to apoptosis that is associated with increased activity of caspase-3 and activation of Bad. TNFα/...
Moreover, TNF-alpha/CHX-induced production of mitochondrial reactive oxygen species (ROS), DNA fragmentation, and caspase-3 activity was dramatically attenuated by using an anti-oxidant, N-acetylcystein, or an inhibitor of complex I of mitochondrial electron transport chain, rotenone. Inhibition of ...
mRNA stability was then examined and cytokine gene transcripts showed a half life of more than 2 h in cultured B-CLL cells and treatment with cycloheximide (CHX) did not affect cytokine transcript levels in B-CLL cells. These results indicate that: steady state levels of each mRNA do not ...
Our data showed that resistance to apoptosis was accompanied by high levels of TIMP-1 expression in part mediated by NF-kappaB activation, whereas under apoptotic conditions, in the presence of cycloheximide (CHX), TIMP-1 and alphavbeta3 integrin protein levels were signi...
Several cofactors can induce and or amplify HIV-1 replication and negatively affect disease progression and pathogenesis. Ethanol consumption is an important risk factor for HIV-1 infection, and it has been implicated in increased HIV-1 replication and progression of infection. Because tumor necrosis ...
In CMVEC from mice and newborn pigs, 15 ng/ml TNF-alpha alone, or with 10 microg/ml cycloheximide (CHX) caused apoptosis detected by nuclear translocation of p65 NF-kappaB, caspase-3 activation, DNA fragmentation, cell-cell contact destabilization, and cell detachment. TNF-alpha did not ...