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Id1 and Id3 are required for neurogenesis, angiogenesis and vascularization of tumour xenografts.Id1和Id3是肿瘤异种移植的神经发生、血管生成和血管化所必需的。
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Id-1 and Id-2 are overexpressed in pancreatic cancer and in dysplastic lesions in chronic pancreatitis.Id-1和Id-2在胰腺癌以及慢性胰腺炎的发育异常病变中过度表达。
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Impaired immune responses and B-cell proliferation in mice lacking the Id3 gene.缺乏Id3基因的小鼠免疫反应受损及B细胞增殖异常。
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Impaired mammary gland development in Cyl-1(-/-) mice during pregnancy and lactation is epithelial cell autonomous.Cyl-1(-/-)小鼠在怀孕和哺乳期间乳腺发育受损是上皮细胞自主性的。
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Prolactin controls mammary gland development via direct and indirect mechanisms.催乳素通过直接和间接机制控制乳腺发育。
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缺乏螺旋-环-螺旋抑制因子Id2的小鼠的泌乳缺陷

Lactation defect in mice lacking the helix-loop-helix inhibitor Id2.

作者信息

Mori S, Nishikawa S I, Yokota Y

机构信息

Department of Molecular Genetics, Kyoto University Graduate School of Medicine, Shogoin Kawahara-cho 53, Sakyo-ku, Kyoto 606-8507, Japan.

出版信息

EMBO J. 2000 Nov 1;19(21):5772-81. doi: 10.1093/emboj/19.21.5772.

DOI:10.1093/emboj/19.21.5772
PMID:11060028
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC305805/
Abstract

Id proteins are thought to be negative regulators of cell differentiation and positive regulators of cell proliferation. Mammary glands of Id2(-/-) 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.

摘要

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。Id2基因敲除雌性小鼠的乳腺在怀孕期间显示出小叶-腺泡发育严重受损。Id2基因敲除的乳腺上皮没有早熟成熟,而是在细胞增殖和细胞存活方面都表现出内在缺陷,这意味着Id2在妊娠乳腺上皮中的作用主要是刺激细胞增殖和维持细胞活力。乳腺发育所需基因的表达研究表明Id2是这些基因的下游或平行因子。在交配后7天的Id2基因敲除乳腺中也观察到Stat5的DNA结合活性降低。我们的结果表明Id2在妊娠乳腺中具有不可或缺的作用。