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a(CHEBI:tamoxifen) -> (cat(p(HGNC:FADD)) -> bp(GO:"G2/M transition of mitotic cell cycle"))
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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We demonstrated here that long-term tamoxifen treatment causes G2/M cell cycle arrest through c-jun N-terminal kinase (JNK) activation, which is dependent on phosphorylation of Fas-associated death domain-containing protein (FADD) at 194 serine in an oestrogen (ER) receptor-positive breast cancer cell line, MCF-7. We conclude that JNK-mediated phosphorylation of FADD plays an important role in the negative regulation of cell growth and metastasis, independent of the ER status of a breast cancer, so that JNK/FADD signals might be promising targets for cancer therapy.
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Selventa
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2014-07-03T14:30:41.350+02:00
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