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Vol. 13, No. 4, pp. 382-387, February 15, 1999

RESEARCH COMMUNICATION
The prosurvival Bcl-2 homolog Bfl-1/A1 is a direct transcriptional target of NF-kappa B that blocks TNFalpha -induced apoptosis

Wei-Xing Zong,1,2 Leonard C. Edelstein,1,2 Cailin Chen,1 Judy Bash,1,3,5 and Céline Gélinas1,4,6

1 Center for Advanced Biotechnology and Medicine, 2 Graduate Program in Biochemistry and Molecular Biology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School (UMDNJ-RWJMS), 3 Graduate Program in Microbiology and Molecular Genetics, Rutgers University, 4 Department of Biochemistry, UMDNJ-RWJMS, Piscataway, New Jersey 08854-5638 USA

Bcl-2-family proteins are key regulators of the apoptotic response. Here, we demonstrate that the pro-survival Bcl-2 homolog Bfl-1/A1 is a direct transcriptional target of NF-kappa B. We show that bfl-1 gene expression is dependent on NF-kappa B activity and that it can substitute for NF-kappa B to suppress TNFalpha -induced apoptosis. bfl-1 promoter analysis identified an NF-kappa B site responsible for its Rel/NF-kappa B-dependent induction. The expression of bfl-1 in immune tissues supports the protective role of NF-kappa B in the immune system. The activation of Bfl-1 may be the means by which NF-kappa B functions in oncogenesis and promotes cell resistance to anti-cancer therapy.

[Key Words: Rel; NF-kappa B; Bfl-1; A1; TNFalpha ; apoptosis]


GENES & DEVELOPMENT 13:382-387 © 1999 by Cold Spring Harbor Laboratory Press  ISSN 0890-9369/99 $5.00

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