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Matches in Nanopublications for { ?s ?p "To test whether XBP1 mediated intestinal inflammation arose from increased JNK activity in a microbiota and cytokine free system, we silenced XBP1 expression in the mouse IEC line MODE-K with a siRNA retrovirus (iXBP) and used flagellin and TNFalpha, as proinflammatory stimulants (Lodes et al., 2004). TNFalpha and flagellin increased JNK phosphorylaton and CXCL1 production from MODE-K.iXBP (50?90% reduction of XBP1) compared to MODE-K.Ctrl cells (Fig. 4CDE) that was dose-dependently and specifically (Supplementary Fig. 5AB) blocked by the JNK inhibitor, SP600125 (Fig. 4FG) but did not affect CD1d-restricted MODE-K antigen presenting function (van de Wal et al., 2003) (Fig. 4H). We conclude that impaired XBP1 expression directly heightens proinflammatory JNK/SAPK signaling in IECs in response to environmental stimuli and may contribute to Paneth, goblet cell and MODE-K.iXBP apoptosis (Fig. 2ACD, Supplementary Fig. 6AB)." ?g. }

• _5 value "To test whether XBP1 mediated intestinal inflammation arose from increased JNK activity in a microbiota and cytokine free system, we silenced XBP1 expression in the mouse IEC line MODE-K with a siRNA retrovirus (iXBP) and used flagellin and TNFalpha, as proinflammatory stimulants (Lodes et al., 2004). TNFalpha and flagellin increased JNK phosphorylaton and CXCL1 production from MODE-K.iXBP (50?90% reduction of XBP1) compared to MODE-K.Ctrl cells (Fig. 4CDE) that was dose-dependently and specifically (Supplementary Fig. 5AB) blocked by the JNK inhibitor, SP600125 (Fig. 4FG) but did not affect CD1d-restricted MODE-K antigen presenting function (van de Wal et al., 2003) (Fig. 4H). We conclude that impaired XBP1 expression directly heightens proinflammatory JNK/SAPK signaling in IECs in response to environmental stimuli and may contribute to Paneth, goblet cell and MODE-K.iXBP apoptosis (Fig. 2ACD, Supplementary Fig. 6AB)." provenance.
• _7 value "To test whether XBP1 mediated intestinal inflammation arose from increased JNK activity in a microbiota and cytokine free system, we silenced XBP1 expression in the mouse IEC line MODE-K with a siRNA retrovirus (iXBP) and used flagellin and TNFalpha, as proinflammatory stimulants (Lodes et al., 2004). TNFalpha and flagellin increased JNK phosphorylaton and CXCL1 production from MODE-K.iXBP (50?90% reduction of XBP1) compared to MODE-K.Ctrl cells (Fig. 4CDE) that was dose-dependently and specifically (Supplementary Fig. 5AB) blocked by the JNK inhibitor, SP600125 (Fig. 4FG) but did not affect CD1d-restricted MODE-K antigen presenting function (van de Wal et al., 2003) (Fig. 4H). We conclude that impaired XBP1 expression directly heightens proinflammatory JNK/SAPK signaling in IECs in response to environmental stimuli and may contribute to Paneth, goblet cell and MODE-K.iXBP apoptosis (Fig. 2ACD, Supplementary Fig. 6AB)." provenance.
• _6 value "To test whether XBP1 mediated intestinal inflammation arose from increased JNK activity in a microbiota and cytokine free system, we silenced XBP1 expression in the mouse IEC line MODE-K with a siRNA retrovirus (iXBP) and used flagellin and TNFalpha, as proinflammatory stimulants (Lodes et al., 2004). TNFalpha and flagellin increased JNK phosphorylaton and CXCL1 production from MODE-K.iXBP (50?90% reduction of XBP1) compared to MODE-K.Ctrl cells (Fig. 4CDE) that was dose-dependently and specifically (Supplementary Fig. 5AB) blocked by the JNK inhibitor, SP600125 (Fig. 4FG) but did not affect CD1d-restricted MODE-K antigen presenting function (van de Wal et al., 2003) (Fig. 4H). We conclude that impaired XBP1 expression directly heightens proinflammatory JNK/SAPK signaling in IECs in response to environmental stimuli and may contribute to Paneth, goblet cell and MODE-K.iXBP apoptosis (Fig. 2ACD, Supplementary Fig. 6AB)." provenance.