Literature DB >> 11715476

[The role of activation of p38 MAPK induced by LPS in TNF-alpha gene expression].

Y Jiang1, A Liu, L Zhang.   

Abstract

OBJECTIVE: To study the molecular mechanisms of TNF-alpha expression induced by LPS for the exploring of novel methods to prevent and treat clinical patients of endotoxic shock.
METHODS: Protein kinase assay was used to detect the kinase activity stimulated by LPS; Confocal laser scan technique was used to show the translocation of p38 on the activation; RT-PCR and reporter gene system were used to study the molecular mechanism of TNF-alpha gene transcription.
RESULTS: In RAW cells, p38 was activated on the stimulation of LPS, and activated p38 moved into nucleus from cytosol. TNF-alpha mRNA increased on the stimulation of LPS and the increased promoter transactivity induced by LPS could be inhibited significantly by specific inhibitor for p38.
CONCLUSION: p38 MAPK was activated on the stimulation of LPS, which brought about its translocation to the nucleus to act on transcription factors to regulate cellular processes. p38 MAPK is an important regulator of TNF-alpha gene expression induced by LPS.

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Year:  1999        PMID: 11715476

Source DB:  PubMed          Journal:  Zhonghua Yi Xue Za Zhi        ISSN: 0376-2491


  1 in total

1.  Modulation of LPS-stimulated pulmonary inflammation by Borneol in murine acute lung injury model.

Authors:  Weiting Zhong; Yiwen Cui; Qinlei Yu; Xianxing Xie; Yan Liu; Miaomiao Wei; Xinxin Ci; Liping Peng
Journal:  Inflammation       Date:  2014-08       Impact factor: 4.092

  1 in total

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