A truncated erythropoietin receptor and cell death: a reanalysis.
A truncated erythropoietin receptor and cell death: a reanalysis.
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截短的促红细胞生成素受体和细胞死亡：重新分析。
DOI：
10.1126/science.8160019
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发表时间：
1994
期刊：
影响因子：
56.9
通讯作者：
H. Nakauchi
中科院分区：
文献类型：
--
作者：
Y. Nakamura;H. Nakauchi
1993年9月27日; 1993年12月14日接受Ba/F3系作为受体细胞。最近，有报道称Ba/F3细胞中表达少量内源性EPOR（3）。其他研究者报道JAK 2激酶通过结合受体的胞质部分在EPOR介导的信号转导中起关键作用（4）。这些观察结果提示我们排除了内源性小鼠EPOR在EPOR-T表达转染子Ba/F3-（EPORT）中负责EPO应答细胞增殖的可能性。出乎意料的是，从EPOR-T转染的Ba/F3细胞获得的mRNA的RT-PCR显示EPOR-T和EPOR-F信使两者的存在（图1A，泳道2）。当这些转染子在EPO下培养一周时，EPOR-F信息的量增加（图1A，泳道3）。PCR产物的亚克隆和测序鉴定该片段为人EPOR-F而不是小鼠内源性EPOR。我们用于构建EPOR-T表达载体（pEPOR-TF）的互补DNA（cDNA）克隆含有一个插入片段，
27 September 1993; accepted 14 December 1993 line, Ba/F3, as recipient cells. Recently, it was reported that a small amount of endogenous EPOR is expressed in Ba/F3 cells (3). Other investigators reported that JAK2 kinase has a critical role in EPOR-mediated signal transduction by binding to the cytoplasmic portion of the receptor (4). These observations prompted us to rule out the possibility that the endoge-nous mouse EPOR isresponsible for EPO-responsive cell proliferation in EPOR-T expressing transfectants, Ba/F3-(EPORT). Unexpectedly, RT-PCR of mRNA obtained from EPOR-T-transfected Ba/F3 cells showed presence of both EPOR-T and EPOR-F messages (Fig. lA, lane 2). When these transfectants were cultured under EPO for a week, the amount of EPOR-F messages increased (Fig. lA, lane 3). Subcloning and sequencing of the PCR products identified this fragment as human EPOR-F rather than mouse en-dogenous EPOR. The complementary DNA (cDNA) clone that we used for construction of an expression vectorfor EPOR-T (pEPOR-TF) contained an in-
促红细胞生成素受体的结构、功能和激活。
影响因子：
20.3
作者：
Youssoufian,H;Longmore,G;Neumann,D;Yoshimura,A;Lodish,HF
通讯作者：
Lodish,HF