The role of 3' poly(A) tail metabolism in tumor necrosis factor-alpha regulation

被引：64

作者：

Crawford, EK

Ensor, JE

Kalvakolanu, I

Hasday, JD

机构：

[1] BALTIMORE VA MED CTR, MED SERV, BALTIMORE, MD 21201 USA

[2] UNIV MARYLAND, SCH MED, DEPT MED, DIV PULM & CRIT CARE MED, BALTIMORE, MD 21201 USA

[3] UNIV MARYLAND, SCH MED, DEPT PATHOL, DIV PULM & CRIT CARE MED, BALTIMORE, MD 21201 USA

[4] UNIV MARYLAND, BALTIMORE CYTOKINE CARE LAB, BALTIMORE, MD 21201 USA

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 1997年 / 272卷 / 34期

关键词：

D O I：

10.1074/jbc.272.34.21120

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

In unstimulated RAW 264.7 macrophage-like cells, tumor necrosis factor-alpha (TNF-alpha) mRNA was transcribed and accumulated in the cytoplasm, but the TNF-alpha transcripts failed to associate with polysomes, and TNF-alpha protein was not detected. Stimulation with lipopolysaccharide(LPS) induced an increase in TNF-alpha transcription, cytoplasmic TNF-alpha mRNA accumulation, polysome association, and secretion of TNF-alpha protein, This process was associated with a 200-nucleotide increase in the apparent length of the TNF-alpha mRNA. The difference in TNF-alpha mRNA size was caused by marked truncation of the 3' poly(A) tail in unstimulated cells. Fully adenylated TNF-alpha mRNA appeared within 15 min of LPS stimulation, We speculate that removal of the poly(A) tail blocks initiation of TNF-alpha translation in unstimulated macrophages LPS inactivates this process, allowing synthesis of translatable polyadenylated TNF-alpha mRNA.

引用

页码：21120 / 21127

页数：8

共 46 条

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