PMID: 9190210Feb 1, 1997Paper

The nfkb1 promoter is controlled by proteins of the Ets family

Molecular Biology of the Cell
P F LambertR R Doherty

Abstract

The gene encoding NFKB1 is autoregulated, responding to NF-kappa B/Rel activation through NF-kappa B binding sites in its promoter, which also contains putative sites for Ets proteins. One of the Ets sites, which we refer to as EBS4, is located next to an NF-kappa B/Rel binding site, kB3, which is absolutely required for activity of the promoter in Jurkat T cells in response to activation by phorbol 12-myristate 13-acetate (PMA), PMA/ionomycin, or the Tax protein from human T cell leukemia virus type I. We show that EBS4 is, required for the full response of the nfkb1 promoter to PMA or PMA/ionomycin in Jurkat cells. EBS4 is bound by Ets-1, Elf-1, and other species. Overexpression of Ets-1 augments the response to PMA/ionomycin and this is reduced by mutation of EBS4. Elf-1 has less effect in conjunction with PMA/ionomycin, but by itself activates the promoter 12-fold. This activation is only partly affected by mutation of EBS4, and a mutant promoter that binds Ets-1, but not Elf-1, at the EBS4 site responds to PMA/ionomycin as efficiently as the wild-type. Ets proteins may be responsible for fine-tuning the activity of the nfkb1 gene in a cell-type-specific manner.

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Citations

Jan 20, 2011·Nature Communications·Vinagolu K RajasekharHoward I Scher
Aug 27, 2010·Journal of Virology·Mei XuDenise A Galloway
Jul 23, 2009·BMC Systems Biology·Johannes WollboldUlrike Gausmann
Nov 5, 2014·Leukemia & Lymphoma·Monica TestoniFrancesco Bertoni
Mar 30, 2016·Drug Discovery Today·Amish Asthana, William S Kisaalita
Feb 15, 2001·Oncogene·V I Sementchenko, D K Watson
Nov 14, 2002·Laboratory Investigation; a Journal of Technical Methods and Pathology·Fanny Baran-MarszakJean Feuillard
Jan 25, 2000·American Journal of Physiology. Regulatory, Integrative and Comparative Physiology·L L ReznikovC A Dinarello
Mar 4, 2006·Molecular Cancer Research : MCR·Pei-Yun Chang, Shigeki Miyamoto

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