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Volume 271, Number 34, Issue of August 23, 1996 pp. 20392-20398
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

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

(Received for publication, March 21, 1996, and in revised form, June 6, 1996)

Florian P. Limbourg , Heike Städtler , G. Chinnadurai , Patrick A. Baeuerle ^§ and M. Lienhard Schmitz

From the Institute of Biochemistry and Molecular Biology, Albert-Ludwigs-University, Hermann-Herder-Strasse, D-79104 Freiburg, Germany, the  Institute for Molecular Virology, St. Louis University Health Sciences Center, St. Louis, Missouri 63110, and ^§ Tularik Inc., South San Francisco, California 94080

The early transcribed adenovirus proteins E1A and E1B display a variety of functions in the transformation of primary rodent cells and the regulation of apoptosis and transcription. We have recently shown recently that the E1B 19 kDa protein from Adenovirus 5 (Ad 5) can functionally antagonize the stimulatory effect of E1A 13S on the human transcription factor NF-B. Here we show that expression of E1B 19 kDa negatively interfered with the activation of NF-B by different stimuli, such as the E1A 13S protein, and treatment with phorbol ester and tumor necrosis factor . This suggests that E1B 19 kDa acts on a common upstream signaling event. Band shift experiments showed that expression of E1B 19 kDa impaired the generation of the nuclear, DNA-binding form of NF-B. Domain mapping experiments employing various E1B 19 kDa mutants revealed the necessity of a hydrophobic Bcl-2 homology region between amino acids 90 and 96 for NF-B inhibition. Co-transfection experiments showed that the inhibitory effect of E1B 19 kDa on E1A 13S-activated NF-B transcription was gradually lost in the course of time. Thus the continuous stimulatory action of E1A 13S can finally override the antagonistic effects of E1B 19 kDa on NF-B activity. In contrast to E1B 19 kDa, expression of the E1B 55 kDa protein did not result in a de novo activation of NF-B, but co-stimulated the transcriptional potential of activated NF-B.

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