SIGNAL TRANSDUCTION BY THE PLATELET-DERIVED GROWTH-FACTOR RECEPTOR
SIGNAL TRANSDUCTION BY THE PLATELET-DERIVED GROWTH-FACTOR RECEPTOR
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DOI：
10.1126/science.2538922
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发表时间：
1989-03-24
期刊：
影响因子：
56.9
通讯作者：
WILLIAMS, LT
中科院分区：
文献类型：
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作者：
WILLIAMS, LT
KI 缺失突变体、羧基末端缺失 (Act) 突变体、ATP 结合位点突变体 (K602A)、跨膜突变体和酪氨酸至苯丙氨酸点突变的构建细节将在别处报道（JA Escobedo 和 LT Williams；JA Escobedo 等人；均在准备中）。在每种情况下，突变体 eDNA 克隆均使用双脱氧核苷酸和 Sequenase 测序系统进行测序。所有突变受体 eDNA 序列都被克隆到表达载体中，处于 SV40 早期启动子的转录控制下，如前所述（Escobedo 等人，1988a）。通过将每个受体突变体的质粒与赋予新霉素抗性的质粒（pSV2neo）共转染来制备稳定的转染子。克隆具有抗性
The details of the construction of the KI deletion mutant, a carboxy-terminal deletion (Act) mutant, the ATP-binding site mutant (K602A), the transmembrane mutants, and the tyrosine-to-phenylalanine point mutations will be reported elsewhere (JA Escobedo and LT Williams; JA Escobedo et al.; both in prep,). In each case, the mutant eDNA clones were sequenced using dideoxy nucleotides and the Sequenase sequencing system. All of the mutated receptor eDNA sequences were cloned into an expression vector under the transcriptional control of the SV40 early promoter as described previously (Escobedo et al. 1988a). Stable transfectants were prepared by cotransfecting plasmids from each receptor mutant with a plasmid that confers resistance to neomycin (pSV2neo). Clones resistant to