The essential role of the UA-rich sequence in endotoxin-induced cachectin/TNF synthesis.

J. Han, B. Beutler

Research output: Contribution to journalArticle

64 Citations (Scopus)

Abstract

Using a series of reporter constructs in which a CAT coding sequence is constitutively transcribed under the influence of the SV40 late promoter but followed by varying portions of the 3'-untranslanted region of TNF, we have shown that the UA-rich element, present in the distal third of the 3'-unstranslated region of TNF, is absolutely required for translational activation of TNF synthesis. Replacement of the UA-rich element by an unrelated sequence of similar length completely abolishes the response. However, the context within which the UA-rich element is presented also appears to be essential, since replacement of flanking portions of 3'-untranslated sequence also blocks the response to LPS. These findings suggest that the primary role of the UA-rich element may consist in its ability to mediate translational activation in response to specific inducing signals.

Original languageEnglish (US)
Pages (from-to)71-75
Number of pages5
JournalEuropean Cytokine Network
Volume1
Issue number2
StatePublished - May 1990

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Endotoxins
Tumor Necrosis Factor-alpha
Chemical activation

ASJC Scopus subject areas

  • Cell Biology
  • Immunology

Cite this

The essential role of the UA-rich sequence in endotoxin-induced cachectin/TNF synthesis. / Han, J.; Beutler, B.

In: European Cytokine Network, Vol. 1, No. 2, 05.1990, p. 71-75.

Research output: Contribution to journalArticle

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