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c-mpl基因缺陷小鼠中的血小板减少症。

Thrombocytopenia in c-mpl-deficient mice.

作者信息

Gurney A L, Carver-Moore K, de Sauvage F J, Moore M W

机构信息

Department of Molecular Biology, Genentech, South San Francisco, CA 94080.

出版信息

Science. 1994 Sep 2;265(5177):1445-7. doi: 10.1126/science.8073287.

Abstract

Thrombopoietin (TPO) is a cytokine that is involved in the regulation of platelet production. The receptor for TPO is c-Mpl. To further investigate the role and specificity of this receptor in regulating megakaryocytopoiesis, c-mpl-deficient mice were generated by gene targeting. The c-mpl-/- mice had an 85 percent decrease in their number of platelets and megakaryocytes but had normal amounts of other hematopoietic cell types. These mice also had increased concentrations of circulating TPO. These results show that c-mpl specifically regulates megakaryocytopoiesis and thrombopoiesis through activation by its ligand TPO.

摘要

血小板生成素(TPO)是一种参与血小板生成调节的细胞因子。TPO的受体是c-Mpl。为了进一步研究该受体在调节巨核细胞生成中的作用和特异性,通过基因靶向技术构建了c-mpl基因缺陷小鼠。c-mpl基因敲除小鼠的血小板和巨核细胞数量减少了85%,但其他造血细胞类型的数量正常。这些小鼠循环中的TPO浓度也有所升高。这些结果表明,c-Mpl通过其配体TPO的激活特异性地调节巨核细胞生成和血小板生成。

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