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Cross‐coupling of the NF‐kappa B p65 and Fos/Jun transcription factors produces potentiated biological function.
Author(s) -
Stein B.,
Baldwin A.S.,
Ballard D.W.,
Greene W.C.,
Angel P.,
Herrlich P.
Publication year - 1993
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1993.tb06066.x
Subject(s) - chapel , center (category theory) , library science , history , art history , computer science , chemistry , crystallography
NF‐kappa B and AP‐1 represent distinct mammalian transcription factors that target unique DNA enhancer elements. The heterodimeric NF‐kappa B complex is typically composed of two DNA binding subunits, NF‐kappa B p50 and NF‐kappa B p65, which share structural homology with the c‐rel proto‐oncogene product. Similarly, the AP‐1 transcription factor complex is comprised of dimers of the c‐fos and c‐jun proto‐oncogene products or of closely related proteins. We now demonstrate that the bZIP regions of c‐Fos and c‐Jun are capable of physically interacting with NF‐kappa B p65 through the Rel homology domain. This complex of NF‐kappa B p65 and Jun or Fos exhibits enhanced DNA binding and biological function via both the kappa B and AP‐1 response elements including synergistic activation of the 5′ long terminal repeat of the human immunodeficiency virus type 1. These findings support a combinatorial mechanism of gene regulation involving the unexpected cross‐coupling of two different classes of transcription factors to form novel protein complexes exhibiting potentiated biological activity.