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

Carballo, Ester, Lai, Wi S., Blackshear, Perry J.·2000·Blood

Abstract

Deficiency of tristetraprolin (TTP), the prototype of the CCCH zinc finger proteins, results in a complex inflammatory syndrome in mice. Most aspects of the syndrome are secondary to excess circulating tumor necrosis factor (TNF)–, a consequence of increased stability of TNF- messenger RNA (mRNA) in TTP-deficient macrophages. TTP can bind directly to the AU-rich element in TNF- mRNA, increasing its lability. Here we show that TTP deficiency also results in increased cellular production of granulocyte-macrophage colony–stimulating factor (GM-CSF) and increased stability of its mRNA, apparently secondary to decreased deadenylation. Similar findings were observed in mice also lacking both types of TNF- receptors, excluding excess TNF- production as a cause of the increased GM-CSF mRNA levels and stability. TTP appears to be a physiological regulator of GM-CSF mRNA deadenylation and stability.

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Metadata

Authors
Carballo, E., Lai, W. S., & Blackshear, P. J.
Venue
Blood
Published
2000-03-15
Volume
95
Issue
6
Pages
1891-1899
ISSN
  • 0006-4971 (ISSN-L)
  • 1528-0020
OpenAlex
W27411732
Cited by
441
References
0
FWCI
7.66
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Evidence that tristetraprolin is a physiological regulator of granulocyte-macrophage colony-stimulating factor messenger RNA deadenylation and stability. https://app.cochat.ai/papers/10.1182/blood.v95.6.1891
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Carballo, E., Lai, W. S., & Blackshear, P. J. (2000). Evidence that tristetraprolin is a physiological regulator of granulocyte-macrophage colony-stimulating factor messenger RNA deadenylation and stability. Blood. https://doi.org/10.1182/blood.v95.6.1891

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