Sentence examples for impairment of expression from inspiring English sources

It was clear that inclusion of M2-encoding sequence resulted in dramatic impairment of expression of the fusion proteins, with NPM1NS1 construct expressing at least 10 times more efficiently than NPM1M2NS1 (Fig. 2A).

Specifically, reduced activation of NF-κB and MAPKs (and associated impairment of expression of cell adhesion molecules) was detected in the lungs of Nod2 −/− mice challenged with Escherichia coli [ 81].

This is somewhat distinct from the effects we have recently reported in respect to the impairment of CD49e expression (which forms the integrin α5β1/VLA-5, another fibronectin receptor), in which we did not find changes in the membrane expression of VLA-4, ascertained by cytofluorometry as well [ 7].

These data indicate a long-lasting impairment of mGlu2/3 expression that may contribute to abnormal presynaptic plasticity, exaggerate glutamate release and hyperexcitability in temporal lobe epilepsy.

Again, an impairment of CD107a expression was also exclusively confirmed for CD56dim NK cells.

Importantly, this is not due to an impairment of Wave2 expression, as its level was unchanged by the treatment.

Moreover, our findings suggest the involvement of the JNK-Akt FOXO1-PDX-1-insulin axis in the impairment of insulin expression, and this pathway may explain parts of the molecular mechanisms of β-cell dysfunction induced by FFAs.

More recently, we also demonstrated that overexpression of MTA1 in vitro could remarkably elevate the capability of spermatogenic tumor cells against heat-induced apoptosis, with a marked impairment of p53 expression [13] [14].

Thus, the reason why we did not observe the formation of disulfide bond-mediated dimers with GluN1 C79A C308A double mutant (Fig. 3 and 4) is not due to the impairment of subunit expression, trafficking or assembly.

The significant reduction in the expression of TNF by TLR2-deficient macrophages infected in vitro and the significant reduction of TNF expression in the lungs of TLR2−/− mice infected with LVS is striking and suggests that the increased susceptibility of TLR2-deficient mice to infection can perhaps be accounted for solely by the impairment of TNF expression in vivo early in the infection.

Targeted impairment of SK2 expression or function significantly inhibited CHIKV infection.