作者: Ester Carballo , Wi S. Lai , Perry J. Blackshear
关键词: Messenger RNA 、 Zinc finger 、 Tumor necrosis factor alpha 、 Granulocyte macrophage colony-stimulating factor 、 ZFP36 、 Receptor 、 Biochemistry 、 Biology 、 Tristetraprolin 、 Cell biology 、 Regulator
摘要: Deficiency of tristetraprolin (TTP), the prototype CCCH zinc finger proteins, results in a complex inflammatory syndrome mice. Most aspects are secondary to excess circulating tumor necrosis factor (TNF)–, consequence increased stability TNF- messenger RNA (mRNA) TTP-deficient macrophages. TTP can bind directly AU-rich element mRNA, increasing its lability. Here we show that deficiency also cellular production granulocyte-macrophage colony–stimulating (GM-CSF) and apparently decreased deadenylation. Similar findings were observed mice lacking both types receptors, excluding as cause GM-CSF mRNA levels stability. appears be physiological regulator deadenylation