Thrombopoietin-Induced Signal Transduction and Potentiation of Platelet Activation
Thrombopoietin-Induced Signal Transduction and Potentiation of Platelet Activation
复制标题
血小板生成素诱导的信号转导和血小板激活的增强
作者：
A. Oda;Y. Miyakawa;B. Druker;K. Ozaki;H. Ohashi;T. Kato;Hiroshi Miyazaki;M. Handa;K. Ikebuchi;Y. Ikeda
血小板生成素是巨核细胞生成和血小板生成的体液调节因子，多年来一直被认为存在，然而，一些研究人员对这种因子的存在持怀疑态度。血小板生成素的现代研究开始于c-mpl（v-mpl癌基因的细胞对应物）及其同源配体基因的克隆。在克隆c-mpl原癌基因后，2 Methia等人3发现，在存在与该基因反义的寡核苷酸的情况下，CD 34+细胞发育成巨核细胞前体的效率较低。由于向其他谱系的发展几乎是完整的，因此有理由认为c-mpl蛋白可能是血小板生成素样因子的受体。3这项研究激发了许多研究，最终在1994年克隆了血小板生成素基因。1，4-8
Introduction The presence of thrombopoietin, a humoral regulator of megakaryopoiesis and thrombopoiesis, had been suggested for years,1 however, some investigators were skeptical about the existence of such a factor. Modern studies of thrombopoietin begin with the cloning of c-mpl (the cellular counterpart of the v-mpl oncogene) and its cognate ligand genes. Following the cloning of the c-mpl proto-oncogene,2 Methia et al3 found that, in the presence of oligonucleotides antisense to the gene, CD34+ cells developed into megakaryocytic precursors less efficiently. As the development into other lineage was nearly intact, it was reasonably argued that the c-mpl protein may be the receptor for a thrombopoietin-like factor.3 This study inspired numerous investigations, which culminated in the cloning of the thrombopoietin gene in 1994.1, 4-8
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影响因子：
20.3
作者：
Drachman, JG;Sabath, DF;Kaushansky, K
通讯作者：
Kaushansky, K
影响因子：
20.3
作者：
Jichun Chen;Lidija Herceg-Harjacek;Jerome E. Groopman;Jadwiga Grabarek
通讯作者：
Jichun Chen;Lidija Herceg-Harjacek;Jerome E. Groopman;Jadwiga Grabarek
影响因子：
20.3
作者：
Gainsford, T;Roberts, AW;Alexander, WS
通讯作者：
Alexander, WS
可溶性血小板生成素受体(Mpl)和粒细胞集落刺激因子受体与钢因子或Flt3/Flk2配体协同作用，直接刺激小鼠原始造血祖细胞的增殖。
影响因子：
20.3
作者：
Ku,H;Hirayama,F;Kato,T;Miyazaki,H;Aritomi,M;Ota,Y;D'Andrea,AD;Lyman,SD;Ogawa,M
通讯作者：
Ogawa,M
DOI：
10.1073/pnas.94.6.2350
发表时间：
1997-03-18
影响因子：
11.1
作者：
Drachman, JG;Kaushansky, K
通讯作者：
Kaushansky, K