Serum stimulation of NIH 3T3 cells induces the production of lipids able to inhibit GTPase-activating protein activity.
Serum stimulation of NIH 3T3 cells induces the production of lipids able to inhibit GTPase-activating protein activity.
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NIH 3T3 细胞的血清刺激诱导产生能够抑制 GTP 酶激活蛋白活性的脂质。
DOI：
10.1128/mcb.10.12.6683-6689.1990
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发表时间：
1990
影响因子：
5.3
通讯作者：
Stacey,DW
中科院分区：
文献类型：
--
作者：
Yu,CL;Tsai,MH;Stacey,DW
在提取细胞总脂质之前，用血清刺激静止的NIH 3T3细胞。将这些脂质在薄层色谱板上进行分离，并检测各个部分抑制gtpase激活蛋白（GAP）活性的能力。制备了两种不同的GAP抑制脂质。在硅胶层析中，一种与花生四烯酸表现相似，而另一种与磷酸肌苷有关。对花生四烯酸相关物质的进一步研究表明，它在血清添加后1至5分钟内产生，但在高密度、接触抑制的培养中从未观察到。这些脂质的身份正在调查中。这些结果提出的可能性，即花生四烯酸的代谢物参与有丝分裂信号传导，这一发现得到了花生四烯酸的几种脂氧合酶产物有效抑制GAP活性的支持。这些结果进一步支持了脂质、GAP和敏感性共同控制细胞增殖的假设。
Quiescent NIH 3T3 cells were stimulated with serum prior to the extraction of total cellular lipids. These lipids were fractionated on thin-layer chromatography plates, and individual fractions were tested for the ability to inhibit GTPase-activating protein (GAP) activity. Two separate GAP inhibitory lipids were produced. One behaved similarly to arachidonic acid during silica gel chromatography, whereas the other was related to a phosphoinositide. Further study of the arachidonic acid-related material indicated that it was produced between 1 and 5 min after serum addition but was never observed in high-density, contact-inhibited cultures. The identity of these lipids is under investigation. The possibility raised by these results, that a metabolite of arachidonic acid is involved in mitogenic signaling, was supported by the finding that several lipoxygenase products of arachidonic acid efficiently inhibited GAP activity. These results provide further support for the hypothesis that lipids, GAP, andrasactivity function together in the control of cellular proliferation.