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Lipopolysaccharide inhibits STAT1. 28 / 28
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28
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"In a human leukemia cell line THP-1, tipifarnib inhibited lipopolysaccharide (LPS)-induced transcription of chemokines [monocyte chemotactic protein (MCP) -1 and MCP-2], cytokines [interleukin (IL)-1beta, IL-6, and interferon (IFN) beta], signaling molecules (MyD88 and STAT-1), proteases [matrix metalloproteinase (MMP-9)], and receptors (urokinase receptor)."
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"It has been reported that LPS stimulation induces suppressor of cytokine signalling 3 (SOCS3) expression and the overexpression of SOCS3 inhibits signal transducer and activator of transcription 1 (STAT1) and janus kinase 1 (JAK1) activation in macrophages treated with IFNgamma 20."
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"In other studies, Shirota and co-workers reported that blockade of STAT1 phosphorylation using synthetic oligonucleotides confers resistance to LPS induced injury whereas Kim et al demonstrated that LPS induced production of the pro inflammatory mediator HMGB1 is attenuated in STAT1 deficient mice."
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"We reported that CBD reduces the activity of the NF-kappaB pathway and upregulates the activation of STAT3 transcription factor in LPS stimulated BV-2 cells, and that both CBD and THC decrease the activation of the LPS induced STAT1 transcription factor, a key player in IFNbeta dependent pro inflammatory processes XREF_BIBR."