A novel sulfonated CNN pincer ligand
has been designed to support
CH and O2 activation at a Pt(II) center. The derived cycloplatinated
aqua complex 7 was found to be one of the most active
reported homogeneous Pt catalysts for H/D exchange between studied
arenes (benzene, benzene-d
6, toluene-d
8, p-xylene, and mesitylene)
and 2,2,2-trifluoroethanol (TFE) or 2,2,2-trifluoroethanol-d; the TON for C6D6 as a substrate
is >250 after 48 h at 80 °C. The reaction is very selective;
no benzylic CH bond activation was observed. The per-CH-bond reactivity
diminishes in the series benzene (19) > toluene (p-CH:m-CH:o-CH = 1:0.9:0.2) >
xylene
(2.9) > mesitylene (1.1). The complex 7 reacts slowly
in TFE solutions under ambient light but not in the dark with O2 to selectively produce a Pt(IV) trifluoroethoxo derivative.
The H/D exchange reaction kinetics and results of the DFT study suggest
that complex 7, and not its TFE derivatives, is the major
species responsible for the arene CH bond activation. The reaction
deuterium kinetic isotope effect, k
H/k
D = 1.7, the reaction selectivity, and reaction
kinetics modeling suggest that the CH bond cleavage step is rate-determining.
The microRNA (miRNA) let-7 is an important miRNA identified in Caenorhabditis elegans and has been shown to be involved in the control of innate immunity. The underlying molecular mechanisms for let-7 regulation of innate immunity remain largely unclear. In this study, we investigated the molecular basis for intestinal let-7 in the regulation of innate immunity. Infection with Pseudomonas aeruginosa PA14 decreased let-7::GFP expression. Intestine- or neuron-specific activity of let-7 was required for its function in the regulation of innate immunity. During the control of innate immune response to P. aeruginosa PA14 infection, SDZ-24 was identified as a direct target for intestinal let-7. SDZ-24 was found to be predominantly expressed in the intestine, and P. aeruginosa PA14 infection increased SDZ-24::GFP expression. Intestinal let-7 regulated innate immune response to P. aeruginosa PA14 infection by suppressing both the expression and the function of SDZ-24. Knockout or RNA interference knockdown of sdz-24 dampened the resistance of let-7 mutant to P. aeruginosa PA14 infection. Intestinal overexpression of sdz-24 lacking 3’-UTR inhibited the susceptibility of nematodes overexpressing intestinal let-7 to P. aeruginosa PA14 infection. In contrast, we could observed the effects of intestinal let-7 on innate immunity in P. aeruginosa PA14 infected transgenic strain overexpressing sdz-24 containing 3’-UTR. In the intestine, certain SDZ-24-mediated signaling cascades were formed for nematodes against the P. aeruginosa PA14 infection. Our results highlight the crucial role of intestinal miRNAs in the regulation of the innate immune response to pathogenic infection.
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