Human fatty acid synthase mRNA: tissue distribution, genetic mapping, and kinetics of decay after glucose deprivation.
Human fatty acid synthase mRNA: tissue distribution, genetic mapping, and kinetics of decay after glucose deprivation.
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发表时间：
1995-07
影响因子：
6.5
通讯作者：
C. Semenkovich;T. Coleman;F. Fiedorek
中科院分区：
文献类型：
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作者：
C. Semenkovich;T. Coleman;F. Fiedorek
为了更好地理解葡萄糖剥夺后发生的脂肪酸合酶（FAS）信息的加速衰减（J. Biol. Chem. 1993. 268：6961-6970），我们表征了HepG 2细胞中人信使的3'末端和FAS mRNA衰减的动力学。FAS基因定位于人染色体17 q24 -25和同线远端小鼠染色体11。FAS信息在人体组织中的表达是普遍存在的，在肝脏、肺和腹内脂肪组织中具有高水平。人mRNA的806个核苷酸的3'非翻译区含有两个具有不稳定性五聚体AUUUA的区域。与含有AUUUA基序的短寿命信息不同，葡萄糖剥夺后FAS mRNA的衰减不是一级的，并且在poly（A）尾中没有可检测到的变化。短暂的葡萄糖剥夺导致FAS信息在密度梯度中比对照信息沉积得更快。在体内治疗与不同的翻译抑制剂表明，翻译本身是不必要的FAS mRNA衰变;协会的多聚核糖体与FAS信息保护它免受衰变。在无细胞衰减实验中，FAS mRNA衰减更快，使用葡萄糖剥夺的组件比葡萄糖处理的细胞。这些数据表明，葡萄糖调节细胞质HepG 2 FAS mRNA的稳定性，通过分配之间的翻译池不受降解和衰变室的消息，功能让人想起其他饮食响应的消息的稳定性调节。
To better understand the accelerated decay of fatty acid synthase (FAS) message that occurs after glucose deprivation (J. Biol. Chem. 1993. 268: 6961-6970), we characterized the 3' terminus of the human message and the kinetics of FAS mRNA decay in HepG2 cells. The FAS gene was localized to human chromosome 17q24-25 and to syntenic distal mouse chromosome 11. Expression of the FAS message in human tissues was ubiquitous with high levels in liver, lung, and intra-abdominal adipose tissue. The 806 nucleotide 3' untranslated region of the human mRNA contained two regions with the instability pentamer AUUUA. Unlike short-lived messages containing AUUUA motifs, FAS mRNA decay after glucose deprivation was not first order, and there were no detectable changes in the poly(A) tail. Glucose deprivation transiently caused FAS message to sediment more rapidly than control message in density gradients. In vivo treatment with different translational inhibitors showed that translation per se was not necessary for FAS mRNA decay; association of polysomes with FAS message protected it from decay. In cell-free decay experiments, FAS mRNA decay was more rapid using components from glucose-deprived than glucose-treated cells. These data suggest that glucose regulates cytoplasmic HepG2 FAS mRNA stability by partitioning the message between a translated pool not subject to degradation and a decay compartment, features reminiscent of regulated stability for other diet-responsive messages.