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RNA-binding protein HuR interacts with thrombomodulin 5 ' untranslated region and represses internal ribosome entry site-mediated translation under IL-1 beta treatment

  1. Author:
    Yeh, C. H.
    Hung, L. Y.
    Hsu, C.
    Le, S. Y.
    Lee, P. T.
    Liao, W. L.
    Lin, Y. T.
    Chang, W. C.
    Tseng, J. T.

  2. Author Address

    Yeh, Chiu-Hung, Hung, Liang-Yi, Chang, Wen-Chang, Tseng, Joseph T.] Natl Cheng Kung Univ, Dept Pharmacol, Tainan 701, Taiwan. [Lee, Pin-Tse] Natl Cheng Kung Univ, Inst Basic Med Sci, Coll Med, Tainan 701, Taiwan. [Hung, Liang-Yi, Liao, Wan-Lin] Natl Cheng Kung Univ, Inst Biosignal Transduct, Tainan 701, Taiwan. [Tseng, Joseph T.] Natl Cheng Kung Univ, Inst Bioinformat, Coll Biosci & Biotechnol, Tainan 701, Taiwan. [Tseng, Joseph T.] Natl Cheng Kung Univ, Ctr Gene Regulat & Signal Transduct Res, Tainan 701, Taiwan. [Hsu, Chin] Kaohsiung Med Univ, Dept Physiol, Grad Inst Physiol & Mol Med, Kaohsiung, Taiwan. [Lin, Yi-Tseng] Kaohsiung Med Univ, Grad Inst Med, Sch Med, Kaohsiung, Taiwan. [Le, Shu-Yun] Natl Canc Inst, Natl Inst Hlth, Ctr Canc Res, Nanobiol Program, Frederick, MD 21702 USA.
    1. Year: 2008
  2. Journal: Molecular Biology of the Cell
    1. 19
    2. 9
    3. Pages: 3812-3822
  4. Type of Article: Article
  1. Abstract:

    Reduction in host-activated protein C levels and resultant microvascular thrombosis highlight the important functional role of protein C anticoagulant system in the pathogenesis of sepsis and septic shock. Thrombomodulin (TM) is a critical factor to activate protein C in mediating the anticoagulation and anti-inflammation effects. However, TM protein content is decreased in inflammation and sepsis, and the mechanism is still not well defined. In this report, we identified that the TM 5' untranslated region (UTR) bearing the internal ribosome entry site (IRES) element controls TM protein expression. Using RNA probe pulldown assay, HuR was demonstrated to interact with the TM 5'UTR. Overexpression of HuR protein inhibited the activity of TM IRES, whereas on the other hand, reducing the HuR protein level reversed this effect. When cells were treated with IL-1 beta, the IRES activity was suppressed and accompanied by an increased interaction between HuR and TM 5'UTR. In the animal model of sepsis, we found the TM protein expression level to be decreased while concurrently observing the increased interaction between HuR and TM mRNA in liver tissue. In summary, HuR plays an important role in suppression of TM protein synthesis in IL-1 beta treatment and sepsis.

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External Sources

  1. PMID: 18579691

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