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The DEXD/H‐box RNA helicase RHII/Gu is a co‐factor for c‐Jun‐activated transcription
Author(s) -
Westermarck Jukka,
Weiss Carsten,
Saffrich Rainer,
Kast Jürgen,
Musti AnnaMaria,
Wessely Matthias,
Ansorge Wilhelm,
Séraphin Bertrand,
Wilm Matthias,
Valdez Benigno C.,
Bohmann Dirk
Publication year - 2002
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 - 10.1093/emboj/21.3.451
Subject(s) - biology , helicase , rna helicase a , transcription factor , transcription factor ii b , transcription factor ii d , microbiology and biotechnology , rna polymerase ii , genetics , transcription (linguistics) , rna , promoter , rna dependent rna polymerase , gene expression , gene , linguistics , philosophy
Tandem affinity purification (TAP) and mass spectrometric peptide sequencing showed that the DEAD‐box RNA helicase RHII/Gu is a functional interaction partner of c‐Jun in human cells. The N‐terminal transcription activation region of, c‐Jun interacts with a C‐terminal domain of RHII/Gu. This interaction is stimulated by anisomycin treatment in a manner that is concurrent with, but independent of, c‐Jun phosphorylation. A possible explanation for this effect is provided by the observation that RHII/Gu translocates from nucleolus to nucleoplasm upon anisomycin or UV treatment or when JNK signaling is activated by overexpression of a constitutively active form of MEKK1 kinase. Several experiments show that the RNA helicase activity of RHII/Gu supports c‐Jun‐mediated target gene activation: dominant‐negative forms of RHII/Gu, as well as a neutralizing antibody against the enzyme, significantly interfered with c‐Jun target gene activity but not with transcription in general. These findings clarify the mechanism of c‐Jun‐mediated transcriptional regulation, and provide evidence for an involvement of RHII/Gu in stress response and in RNA polymerase II‐catalyzed transcription in mammalian cells.