Search alternatives:
significantly mediate » significantly mediated (Expand Search), significantly predicted (Expand Search), significantly mitigated (Expand Search)
mediate decrease » mean decrease (Expand Search), mediated defense (Expand Search)
linear decrease » linear increase (Expand Search)
a decrease » _ decrease (Expand Search), _ decreased (Expand Search), _ decreases (Expand Search)
significantly mediate » significantly mediated (Expand Search), significantly predicted (Expand Search), significantly mitigated (Expand Search)
mediate decrease » mean decrease (Expand Search), mediated defense (Expand Search)
linear decrease » linear increase (Expand Search)
a decrease » _ decrease (Expand Search), _ decreased (Expand Search), _ decreases (Expand Search)
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Data for Figs 8A–8H, 9A–9K, 10A–10I.
Published 2024“…Further research showed that UL4 promoted the phosphorylation levels of SYK and JNK to enhance the ASC phosphorylation, which led to the increase of ASC oligomerization, thus promoting the activation of NLRP3 and AIM2 inflammasome and enhanced GSDMD-mediated pyroptosis. In <i>vivo</i> experiments further showed that PRV UL4 (<sup>132</sup>DVAADAAAEAAAAE<sup>145</sup>) mutated strain (PRV-UL4<sup>mut</sup>) infection did not lead to a significant decrease in viral titers at 12 h. p. i, but it induced lower levels of IL-1β, IL-18, and GSDMD-NT, which led to an alleviated inflammatory infiltration and pathological damage in the lungs and brains, and a lower death rate compared with wild-type PRV strain infection. …”
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Inhibition of PGAM5 and apoptosis prevented <i>T. spiralis</i> larval invasion of Caco-2 monolayer.
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rTsSPc interacted with PGAM5 and increased its protein expression in Caco-2 cells.
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Apoptosis inhibitor abolished and restored rTsSPc-disrupted Caco-2 monolayer barrier integrity.
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PGAM5 knockdown prevented rTsSPc from disrupting Caco-2 monolayer integrity.
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Inhibition of PGAM5 and apoptosis alleviated the rTsSPc-damaged Caco-2 monolayer barrier integrity.
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Downregulation of TRIM37 expression exacerbates pathological damage in the MS model.
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Overexpression <i>TRIM37</i> enhances PEX5 protein stability by promoting PEX5 monoubiquitination.
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