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Ar punctate GFP signals corresponding to the typical Golgi localization pattern (Gao et al., 2012, 2014a). However, strong vacuolar GFP signals were detected after knockdown of -COP by DEX induction, suggesting mislocalization of AtEMP12-GFP-RNIKCD to the vacuole (Figure 7B). These results are consistent with previous transient expression results showing mislocalization of AtEMP12-GFP to post-Golg
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Fficult to predict optima or outcomes (Lazzaro and Small, 2009). The proof that various genes control illness resistance and tolerance was initially obtained from plant research, which demonstrated that genetic variation in each resistance and tolerance existed (Simms and Triplett, 1995). Gene variants that confer higher resistance to pathogens are predicted to be unlikelyto visit fixation inside
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Ar punctate GFP signals corresponding to the typical Golgi localization pattern (Gao et al., 2012, 2014a). However, strong vacuolar GFP signals were detected after knockdown of -COP by DEX induction, suggesting mislocalization of AtEMP12-GFP-RNIKCD to the vacuole (Figure 7B). These results are consistent with previous transient expression results showing mislocalization of AtEMP12-GFP to post-Golg
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Released from necrotic cells and subsequently activates IL-1R1 present at the surface of mesothelial cells. This was proposed to be the prime event inducing neutrophil infiltration and peritoneal inflammation rather than the HMGB1 pathway.152,153 This proinflammatory role of IL-1 was recently confirmed in a mouse model of acute colon inflammation (dextran sodium sulfate-induced colitis), where epi
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