Abstract:
:Despite the essential role of the fibrinogen gamma-chain as a blood clotting factor, the fibrinogen gamma-chain contains a number of interaction sites to recruit other factors such as leukocytes important for prevention of pathogen entry and propagation of the repair process. Interleukin-6 (IL-6) is known as the major inducer of gamma-fibrinogen synthesis in hepatocytes, whereas IL-1beta has been shown to act as a potent inhibitor of gamma-fibrinogen expression. Studies on the rat fibrinogen gamma-chain promoter suggest that nuclear factor (NF)-kappaB replaces the signal transducer and activator of transcription (STAT) 3 from binding to overlapping NF-kappaB/STAT3 binding sites within the 5' regulatory region of the rat gamma-chain gene promoter. However, despite its physiological relevance, the underlying mechanism responsible for the inhibitory effect of IL-1beta in humans is still not understood and apparently more complex. In contrast to the mechanism described for the rat gene our results indicate that IL-1beta suppresses the IL-6-induced activation of the human gamma-fibrinogen gene particularly by blocking the late phase STAT3-tyrosine phosphorylation NF-kappaB-dependently but independent from de novo protein synthesis. Consequently, blocking NF-kappaB activation restores specifically late phase STAT3 activation as well as the induction of the human gamma-fibrinogen gene. In contrast, specifically early STAT3 activation could be restored by a block of the p38 mitogen-activated protein kinase (p38(MAPK)) pathway. In summary, our results indicate that expression of the gamma-fibrinogen gene is mainly controlled by the strength of late phase STAT3 activation, which in turn is negatively regulated by the extent of IL-1beta-mediated NF-kappaB activity.
journal_name
Cell Signaljournal_title
Cellular signallingauthors
Albrecht U,Yang X,Asselta R,Keitel V,Tenchini ML,Ludwig S,Heinrich PC,Häussinger D,Schaper F,Bode JGdoi
10.1016/j.cellsig.2007.04.007subject
Has Abstractpub_date
2007-09-01 00:00:00pages
1866-78issue
9eissn
0898-6568issn
1873-3913pii
S0898-6568(07)00121-0journal_volume
19pub_type
杂志文章abstract::Growing evidence shows that chronic inflammation drives the progression of colorectal cancer (CRC). Cyclooxygenase-2 (COX-2) is one of the most important inflammatory genes involved in solid tumor metastasis. Epidermal growth factor receptor (EGFR) also plays a key role in cancer cell development. We compared the expr...
journal_title:Cellular signalling
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journal_title:Cellular signalling
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journal_title:Cellular signalling
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journal_title:Cellular signalling
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journal_title:Cellular signalling
pub_type: 杂志文章,评审
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journal_title:Cellular signalling
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doi:10.1016/j.cellsig.2008.05.017
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2005.12.009
更新日期:2006-10-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
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journal_title:Cellular signalling
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doi:10.1016/j.cellsig.2019.04.008
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journal_title:Cellular signalling
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journal_title:Cellular signalling
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journal_title:Cellular signalling
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doi:10.1016/j.cellsig.2013.05.014
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