Lactation defect in mice lacking the helix-loop-helix inhibitor Id2
Lactation defect in mice lacking the helix-loop-helix inhibitor Id2
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DOI：
10.1093/emboj/19.21.5772
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发表时间：
2000-11-01
期刊：
影响因子：
11.4
通讯作者：
Yokota, Y
中科院分区：
文献类型：
--
作者：
Mori, S;Nishikawa, SI;Yokota, Y
Id蛋白被认为是细胞分化的负调节因子和细胞增殖的正调节因子。ITd 2（-/-）雌性小鼠的乳腺显示妊娠期间小叶-肺泡发育严重受损。Id 2（-/-）乳腺上皮细胞没有表现出早熟成熟，而是表现出细胞增殖和细胞存活的内在缺陷，这意味着Id 2在妊娠乳腺上皮细胞中的作用主要是刺激细胞增殖和支持细胞活力。乳腺发育所需基因的表达研究表明，Id 2是这些基因的下游或平行因子。交配后7天，在Id 2（-/-）乳腺中也观察到Stat 5的DNA结合活性降低。我们的研究结果表明Id 2在妊娠乳腺中起着不可或缺的作用。
Id proteins are thought to be negative regulators of cell differentiation and positive regulators of cell proliferation. Mammary glands of ITd2(-/-) female mice reveal severely impaired lobulo-alveolar development during pregnancy. Id2(-/-) mammary epithelia show no precocious maturation, but instead exhibit intrinsic defects in both cell proliferation and cell survival, implying that the role of Id2 in pregnant mammary epithelia is mainly stimulation of cell proliferation and support of cell viability. Expression studies of genes required for mammary gland development suggest Id2 to be a downstream or parallel factor of these genes. A decrease in the DNA binding activity of Stat5 was also observed in Id2(-/-) mammary glands at 7 days post-coitus. Our results indicate an indispensable role of Id2 in pregnant mammary glands.