analysis of molecular mechanism of hematopoiesis and hematological disorders

在这个项目中，我们澄清了以下几点：1.Stat1和Stat3被促红细胞生成素（EPO）激活，并在EPO诱导的红细胞分化中充当负调节因子（JBC 272：16507，1997；Blood 92：462，1998）。2.酪氨酸激酶Fes和JAK2激活Stat1和Stat3（手稿于3.Stat3参与红细胞生成和巨核细胞生成中骨髓抑制的恢复（手稿正在准备中）。4． Stat3对血小板生成素（TPO）诱导的巨核细胞分化有负面影响（手稿正在准备中）。5． EPO和TPO信号通路之间存在串扰（手稿正在准备中）。6．丝裂原激活蛋白激酶、Erk-1 和 Erk-2 可能是细胞命运决定向红细胞和巨核细胞谱系的关键因素（Int. Hematol.，出版中）。6． EPO 受体和GATA-1 在红白血病细胞中高度表达(Exp. Hematol. 26: 1148, 1998)。7． FKHRL1 是 EPO 信号转导中 PI3K-Akt 激活途径的下游靶分子之一（新闻中的血液）。

In this project, we clarified several things as follows;1.Stat1 and Stat3 are activated by erythropoietin (EPO) and function as negative regulators in EPO-induced erythroid differentiation (JBC 272: 16507, 1997; Blood 92: 462, 1998).2.Tyrosine kinases Fes and JAK2 activates Stat1 and Stat3 (manuscript in preparation).3.Stat3 is involved in recovery from myelosupression in erythropoiesis and megakaryopoiesis (manuscript in preparation).4. Stat3 has a negative effect on thrombopoietin (TPO)-induced megakaryocytic differentiation (manuscript in preparation.).5. There is a crosstalk between EPO and TPO signaling pathways (manuscript in preparation).6. Mitogen-activated protein kinases, Erk-1 and Erk-2 functions as a possible key factor for cell fate determination toward erythroid and megakaryocytic lineages (Int. Hematol., in press).6. EPO receptor and GATA-1 are highly expressed in erythroleukemia cells (Exp. Hematol. 26: 1148, 1998).7. FKHRL1 is one of downstream target molecules of PI3K-Akt activation pathway in EPO signal transduction (Blood in press).