Evidence that tristetraprolin is a physiological regulator of granulocyte-macrophage colony-stimulating factor messenger RNA deadenylation and stability.

作者: Ester Carballo , Wi S. Lai , Perry J. Blackshear

DOI: 10.1182/BLOOD.V95.6.1891

关键词: Messenger RNAZinc fingerTumor necrosis factor alphaGranulocyte macrophage colony-stimulating factorZFP36ReceptorBiochemistryBiologyTristetraprolinCell biologyRegulator

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

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