The ΔyopPH, ΔyopPE, ΔyopPM, and ΔyopPQ mutants induced the weakest CD8 T cell response and did not significantly protect mice against Listeria presumably due to the strong attenuation of these strains in the mouse model.
In a second experiment, the 5 top ranked mutants plus the 2 mutants inducing the lowest protection were reassessed using 10 mice per group.
Remarkably, the expression of the ΔLOXL2 and H626/628Q mutants induced the same phenotypic effect than wild-type LOXL2 (Fig. 5B, bottom two left panels).
As expected, pVHL missense mutants induced the proteasome-dependent proteolysis of HIF-1α, and this proteolysis was inhibited by MG132 (Fig. 4c and d).
We found that expression of both ΔKH and ΔRGG mutants induces the formation of dFMRP granules in >50% of transfected cells (Fig. 1C, Fig. 2).
Nevertheless, our results indicate that the expression of GFP-dFMRP and of its ΔKH and ΔRGG mutants induces the recruitment of a significant amount of mRNA in dFMRP granules.
Remarkably, the VSV matrix mutant induced the upregulation of major histocompatibility class-I antigen at the tumor cell surface thus favoring recognition by CD8+ T cells.
It is likely that the high level of H2O2 in this mutant induces the HR and increases the resistance to pathogens.
The NYVAC-C-KC-ΔB19R mutant induced the expression of IFN genes, as well as genes involved with antigen processing and presentation genes including the proteasome pathway (figure 4).
We observed that M2 and the M2Y129F mutant induced the phosphorylation of several proteins of approximately 52, 54, 56, 75, 95 (likely Vav1 itself) and 150 kDa (Fig. 2B, fifth panel from top).
