The intranuclear prolactin/cyclophilin B complex as a transcriptional inducer
The intranuclear prolactin/cyclophilin B complex as a transcriptional inducer
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DOI：
10.1073/pnas.092160699
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发表时间：
2002-05-14
影响因子：
11.1
通讯作者：
Clevenger, CV
中科院分区：
文献类型：
--
作者：
Rycyzyn, MA;Clevenger, CV
受体内化后肽类激素（例如促生长激素催乳素）的核易位已被广泛报道。催乳素已被证明与亲环蛋白 13 相互作用，亲环蛋白 13 是亲免蛋白家族的成员。亲环蛋白 B 与催乳素的相互作用增强了催乳素诱导的增殖、细胞生长和催乳素的核逆转运。这些效应可以通过去除亲环蛋白 B 的肽基脯氨酰异构酶活性来消除。我们的研究结果表明，核内催乳素/亲环蛋白 B 复合物通过直接与 Stat5 相互作用而充当转录诱导剂，导致激活 Stat 3 的 Stat 阻遏蛋白抑制剂 (PIAS3) 的去除，从而增强 Stat5 DNA 结合活性和催乳素诱导的 Stat5 介导的基因表达。
The nuclear translocation of peptide hormones, such as the somatolactogenic hormone prolactin, after receptor internalization has been widely reported. Prolactin has been demonstrated to interact with cyclophilin 13, a member of the immunophilin family of proteins. Cyclophilin B interaction with prolactin potentiated prolactin-induced proliferation, cell growth, and the nuclear retrotransport of prolactin. These effects could be abrogated by the removal of the peptidyl-prolyl isomerase activity of cyclophilin B. Our findings indicate that the intranuclear prolactin/cyclophilin B complex acts as a transcriptional inducer by interacting directly with Stat5, resulting in the removal of the Stat-repressor protein inhibitor of activated Stat 3 (PIAS3), thereby enhancing Stat5 DNA-binding activity and prolactin-induced, Stat5-mediated gene expression.