A Hydrophobic Region within the Adenovirus E1B 19 kDa Protein Is Necessary for the Transient Inhibition of NF-κB Activated by Different Stimuli

Adenovirus E1B 19,000-Molecular-Weight Protein Activates c-Jun N-Terminal Kinase and c-Jun-Mediated Transcription

“…Similarly, the activation of GAL4-cJun-mediated transcription by E1B 19K does not appear to be related to its ability to inhibit NF-B activity, since the mutant E1B 19K 123,124 WR-AS was defective in inducing both JNK activation and GAL4-c-Jun-dependent transcription ( Fig. 9A and C) but is fully active in NF-B inhibition (39). Currently, we are investigating whether activation of JNK and c-Junmediated transcription by E1B 19K may play a role in adenoviral lytic infection.…”

“…As mentioned earlier, E1B 19K cooperates with E1A in transformation assays (8,60,66), probably due to its ability to inhibit apoptosis (8,49,60,66). To determine whether the induction of GAL4-c-Jun-mediated transcription by E1B 19K contributes to its ability to inhibit apoptosis and to induce transformation, we tested several previously described E1B 19K transformation-defective mutants for their abilities to induce c-Jun-mediated transcription (8,39,60,66). As shown in Fig.…”

Hydrogen peroxide-induced apoptosis is CD95-independent, requires the release of mitochondria-derived reactive oxygen species and the activation of NF-κB

“…Some of the anti-apoptotic eects of E1B 19K can be explained by functional interactions with the proapoptotic proteins Bax and Nbk/Bik (Han et al, 1996). Another important feature of Bcl-2 and E1B 19K is their ability to counteract the transcriptional activity of NF-kB (Grimm et al, 1996;Schmitz et al, 1996;Limbourg et al, 1996), a characteristic that might contribute to their protective role in H 2 O 2 -induced apoptosis. The inhibition of NF-kB by transient or stable overexpression of IkB-a also prevented cell death, directly showing the involvement of this transcription factor in the onset of apoptosis.…”

The Adenovirus E3 Promoter Is Sensitive to Activation Signals in Human T Cells

“…5 in that the E1A 289R protein (which contains the TAD) could increase basal transcription of E3 while E1A 243R inhibits NF-B-dependent transactivation of E3. It is interesting that while the E1A 289R protein in isolation can increase NF-B-dependent promoter transactivation (52,63), we see no evidence of this cooperation. This could indicate that the default pathway is for 289R to act through AP-1 and not NF-B and/or that inhibition of NF-B-dependent transactivation by 243R is more potent than activation by 289R.…”

“…The 243R E1A protein potently inhibits NF-B-dependent promoter transactivation (15,30,39,59,64), whereas the 289R isoform is generally found to activate these processes (52,63). All of the above-cited studies were performed by transfection of an isolated E1A isoform in the absence of adenovirus infection, so the combined effect of both isoforms expressed during infection remains unknown.…”