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作为生长、细胞凋亡和乳腺发育调节因子的信号转导及转录激活因子

Signal transducers and activators of transcription as regulators of growth, apoptosis and breast development.

作者信息

Bromberg J

机构信息

Rockefeller University and Memorial Sloan Kettering Cancer Center, 1230 York Avenue, New York, NY 10021, USA.

出版信息

Breast Cancer Res. 2000;2(2):86-90. doi: 10.1186/bcr38. Epub 2000 Jan 28.

DOI:10.1186/bcr38
PMID:11250696
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC139428/
Abstract

STAT transcription factors were discovered 10 years ago as mediators of interferon-induced gene expression. They now form an important group, comprising seven members, that are activated by virtually every cytokine and growth factor. Their critical role in development and normal cell signaling has been largely determined through the analysis of transgenic mice lacking individual STAT genes. In addition, cell culture work has further delineated their importance in cellular transformation, apoptosis, differentiation and growth control. This review discusses the specific phenotypes of STAT-deficient animals with a focus on STAT5 and STAT3, as these two STAT molecules are required for normal breast development and involution, respectively, and may play an important role in breast carcinogenesis.

摘要

信号转导和转录激活因子(STAT)转录因子于10年前作为干扰素诱导基因表达的介质被发现。它们现在构成了一个重要的家族,由七个成员组成,几乎可被每种细胞因子和生长因子激活。通过对缺乏单个STAT基因的转基因小鼠的分析,很大程度上确定了它们在发育和正常细胞信号传导中的关键作用。此外,细胞培养研究进一步阐明了它们在细胞转化、凋亡、分化和生长控制中的重要性。本综述讨论了STAT缺陷动物的特定表型,重点是STAT5和STAT3,因为这两种STAT分子分别是正常乳腺发育和退化所必需的,并且可能在乳腺癌发生中起重要作用。

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本文引用的文献

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Suppression of epithelial apoptosis and delayed mammary gland involution in mice with a conditional knockout of Stat3.Stat3条件性敲除小鼠上皮细胞凋亡受抑制及乳腺退化延迟
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Interactions in the transcriptional regulation exerted by Stat5 and by members of the steroid hormone receptor family.Stat5 与类固醇激素受体家族成员在转录调控中所发挥的相互作用。
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ErbB receptor-induced activation of stat transcription factors is mediated by Src tyrosine kinases.表皮生长因子受体(ErbB)诱导的信号转导和转录激活因子(Stat)转录因子激活是由Src酪氨酸激酶介导的。
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