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ELL binding regulates U19/Eaf2 intracellular localization, stability, and transactivation
Author(s) -
Xiao Wuhan,
Jiang Feng,
Wang Zhou
Publication year - 2005
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.20309
Subject(s) - transactivation , transcription factor , myeloid leukemia , biology , prostate cancer , cancer research , microbiology and biotechnology , genetics , gene , cancer
BACKGROUND U19/Eaf2, an androgen‐response gene, is downregulated in advanced human prostate cancer specimens and its overexpression can markedly induce apoptosis in prostate cancer cells. Eleven‐nineteen Lysine‐rich Leukemia (ELL) is an RNA polymerase II transcription elongation factor, initially identified as a fusion partner gene of MLL in the t(11; 19) (q23; p13.1) chromosomal translocation in acute myeloid leukemia. U19/Eaf2 was previously reported as an ELL‐associated factor, a potential transcription factor binds to ELL, forming nuclear speckles in vivo. These findings suggest that ELL–U19/Eaf2 interaction is potentially important in prostate cancer progression and/or acute myeloid leukemia. However, the functional significance of U19/Eaf2 interaction with ELL remains unclear. METHODS Using co‐transfection, co‐immunoprecipitation, protein stability assay and transactivation assay, we characterized the consequence of ELL binding to U19/Eaf2. RESULTS We provide further evidence for U19/Eaf2 as a transcription factor and show that ELL binding is required for nuclear speckle formation of human U19/Eaf2, stabilizes U19/Eaf2 and enhances its transactivation activity. CONCLUSIONS The above observations indicate ELL may be an important factor required for U19/Eaf2 function because U19/Eaf2 nuclear localization and transactivation activity are essential for its function as a transcription factor. Published 2005 Wiley‐Liss, Inc.