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转化生长因子β基因敲除小鼠和显性负性受体转基因小鼠。

TGF-beta knockout and dominant-negative receptor transgenic mice.

作者信息

Letterio J J, Böttinger E P

机构信息

Laboratory of Chemoprevention, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-5055, USA.

出版信息

Miner Electrolyte Metab. 1998;24(2-3):161-7. doi: 10.1159/000057365.

Abstract

Use of homologous recombination and transgenic technologies have provided mouse models to study the physiological roles of the three mammalian TGF-beta isoforms, and their regulation in the context of the intact animal. Mice harboring null mutations for TGF-beta isoforms demonstrate that each exerts discrete nonoverlapping functions during development. TGF-beta1 null mice reveal a crucial role for this cytokine in modulation of the immune system, with evidence for altered development, activation and function of various immune cell populations. New approaches to tissue- and cell-restricted disruption of TGF-beta signaling pathways in transgenic mice carrying dominant-negative mutant TGF-beta receptors will be discussed.

摘要

同源重组和转基因技术的应用为研究三种哺乳动物转化生长因子-β(TGF-β)亚型的生理作用及其在完整动物体内的调节提供了小鼠模型。携带TGF-β亚型无效突变的小鼠表明,每种亚型在发育过程中发挥着独特且不重叠的功能。TGF-β1无效小鼠揭示了这种细胞因子在调节免疫系统中的关键作用,有证据表明各种免疫细胞群体的发育、激活和功能发生了改变。将讨论在携带显性负性突变TGF-β受体的转基因小鼠中对TGF-β信号通路进行组织和细胞特异性破坏的新方法。

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