Alternative forms of the human G-CSF receptor function in growth signal transduction.
Alternative forms of the human G-CSF receptor function in growth signal transduction.
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人类 G-CSF 受体的替代形式在生长信号转导中发挥作用。
DOI：
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发表时间：
1991
期刊：
影响因子：
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通讯作者：
C. Smith
中科院分区：
文献类型：
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作者：
S. Ziegler;T. Davis;J. Schneringer;T. Franklin;T. Tough;M. Teepe;A. Larsen;D. Williams;C. Smith
人粒细胞集落刺激因子（G-CSF）受体（HuG-CSFR）的两种形式，不同的只是在羧基末端，最近被确定的cDNA克隆。在这份报告中，我们表明，在白细胞介素-3（IL-3）依赖性小鼠细胞系BAF/BO 3中转染和随后表达的cDNA克隆将细胞转化为G-CSF反应性。转染的细胞以与天然受体不可区分的方式结合HuG-CSF。在BAF/BO 3细胞中表达胞质结构域缺失的HuG-CSFR突变体形式未能将细胞转化为HuG-CSF反应性。以类似的方式，这两种HuG-CSFRs在白细胞介素-6（IL-6）依赖性鼠杂交瘤B 9中的表达导致这些细胞能够在HuG-CSF中生长[校正]。这些结果有力地表明，HuG-CSFR的胞质结构域的前96个氨基酸中的序列是响应于配体结合的信号转导所需的。
Two forms of the human granulocyte colony-stimulating factor (G-CSF) receptor (HuG-CSFR), differing only at the carboxyl terminus, were recently identified by cDNA cloning. In this report we show that transfection and subsequent expression of either cDNA clone in the interleukin-3 (IL-3)-dependent murine cell line BAF/BO3 converts the cells to G-CSF-responsiveness. The transfected cells bound HuG-CSF in a manner indistinguishable from the native receptors. Expression of a mutant form of the HuG-CSFR, with a deletion in the cytoplasmic domain, in BAF/BO3 cells failed to convert the cells to HuG-CSF-responsiveness. In a similar manner, expression of these two HuG-CSFRs in the interleukin-6 (IL-6)-dependent murine hybridoma B9 resulted in the ability of these cells to grow in HuG-CSF [corrected]. These results strongly suggest that sequences in the first 96 amino acids of the cytoplasmic domain of the HuG-CSFR are required for signal transduction in response to ligand binding.