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Cross‐inhibition of both estrogen receptor α and β pathways by each dominant negative mutant
Author(s) -
Ogawa Sumito,
Inoue Satoshi,
Orimo Akira,
Hosoi Takayuki,
Ouchi Yasuyoshi,
Muramatsu Masami
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)00079-9
Subject(s) - transactivation , estrogen receptor , mutant , estrogen receptor alpha , transcription (linguistics) , transcription factor , estrogen receptor beta , nuclear receptor , chemistry , wild type , receptor , estrogen , microbiology and biotechnology , hormone response element , biology , gene , endocrinology , biochemistry , genetics , philosophy , cancer , breast cancer , linguistics
Both estrogen receptor α (ERα) and the recently identified ERβ are nuclear receptors that are activated by estrogen. It was reported that ERα and ERβ form heterodimers. Here, we show that they activate transcription independently rather than synergistically via estrogen response elements (ERE). To show the cross‐talk between ERα and ERβ, we utilized dominant negative mutants of ERs constructed by C‐terminal truncation. Interestingly, ERα1–530 inhibited transactivation not only by ERα but also by ERβ, whereas ERβ1–481 inhibited transactivation by ERα as well as by ERβ. The GST pull‐down assay also demonstrated the cross‐interaction of these mutants with wild‐type ERα and ERβ. Thus, we found dominant negative mutants that block both ERα and ERβ signaling pathways.