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Mrp8 and Mrp14 are endogenous activators of Toll-like receptor 4, promoting lethal, endotoxin-induced shock
It is demonstrated that mice lacking Mrp8-Mrp14 complexes are protected from endotoxin-induced lethal shock and Escherichia coli–induced abdominal sepsis, indicating new inflammatory components that amplify phagocyte activation during sepsi upstream of TNFα–dependent effects.
Influenza virus propagation is impaired by inhibition of the Raf/MEK/ERK signalling cascade
It is shown that infection of cells with influenza A virus leads to biphasic activation of the Raf/MEK/ERK cascade, which seems to be essential for virus production and RNP export from the nucleus during the viral life cycle.
The Epidermal Growth Factor Receptor (EGFR) Promotes Uptake of Influenza A Viruses (IAV) into Host Cells
- T. Eierhoff, Eike R Hrincius, U. Rescher, S. Ludwig, C. Ehrhardt
- BiologyPLoS pathogens
- 1 September 2010
First indications for an interplay of IAV with receptor tyrosine kinases (RTKs) with representative RTK family-members the epidermal growth factor receptor (EGFR) and the c-Met receptor were studied, showing that these receptors transmit entry relevant signals upon virus binding.
Bivalent role of the phosphatidylinositol‐3‐kinase (PI3K) during influenza virus infection and host cell defence
Investigation of the function of PI3K during influenza virus infection revealed that it appears to regulate a very early step during viral entry, a perfect example of a seemingly antiviral signalling component that is misused by the virus to support effective replication.
IFN‐α antagonistic activity of HCV core protein involves induction of suppressor of cytokine signaling‐3
- J. Bode, S. Ludwig, D. Häussinger
- Biology, MedicineFASEB journal : official publication of the…
- 1 March 2003
It is shown that overexpression of HCV core protein inhibits IFN‐α‐induced tyrosine phosphorylation and activation of STAT1 in hepatic cells, and may be part of the molecular basis ofIFN‐a unresponsiveness in about one‐half of chronically infected HCV‐patients.
Influenza A Virus NS1 Protein Activates the PI3K/Akt Pathway To Mediate Antiapoptotic Signaling Responses
A novel mode of action of the NS1 protein to suppress apoptosis induction is presented and it is shown that NS1 not only blocks but also activates signaling pathways to ensure efficient virus replication.
Caspase 3 activation is essential for efficient influenza virus propagation
It is found that caspase 3 activation during the onset of apoptosis is a crucial event for efficient influenza virus propagation, and poor replication efficiencies of influenza A viruses in cells deficient for caspases could be boosted 30‐fold by ectopic expression of the protein.
Influenza A Virus Inhibits Type I IFN Signaling via NF-κB-Dependent Induction of SOCS-3 Expression
Data is presented indicating that influenza A viruses not only suppress IFNβ gene induction but also inhibit type I IFN signaling through a mechanism involving induction of the suppressor of cytokine signaling-3 (SOCS-3) protein.
MRP8 and MRP14 control microtubule reorganization during transendothelial migration of phagocytes.
The complex of MRP8/MRP14 is the first characterized molecular target integrating MAPK- and calcium-dependent signals during migration of phagocytes, and is confirmed by the fact that MAPK p38 fails to stimulate migration of MRp14(-/-) granulocytes in vitro and MRP14(/-) mice show a diminished recruitment of granulocyte into the granulation tissue during wound healing in vivo.
Rho proteins and the p38-MAPK pathway are important mediators for LPS-induced interleukin-8 expression in human endothelial cells.
The data suggest that LPS-induced NF-kappaB activation and IL-8 synthesis in HUVECs are regulated by both a Rho-dependent signaling pathway and the MKK6/p38 kinase cascade.