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Despite the fact that wild-type and G mutants induced a stronger gp33-specific immune response compared to the MM51R mutant, all VSV strains showed a similar capacity to slow down tumor progression.

All mutations changed the way the protein interacted with the lipid membrane, and selected mutants induced a variety of conformational changes in both p110α and its interaction p85α.

All of these mutants induced a strong reduction of stress fibres in the majority of HeLa cells, and a rounded phenotype with branched protrusions (branching) in 30 40% of cells.

As expected, WT and non-lethal Fam20C mutants (T268M and P328S), but none of the other mutants induced a mobility shift in OPN, consistent with previous reports (Tagliabracci et al., 2012, 2014).

When formulated with alum, the monomeric cysteine mutants induced a similar immune response as the aggregated parental allergens, which is in contrast with data published on Bet v 1.

Similar(55)

Npro deletion mutants induced an increase in DC maturation and IFN-α/β production for both ncp and cp viruses despite reduced replication efficiency in the DC.

Interestingly, eEF1A1 S21 mutants induced an increase of early apoptosis whereas eEF1A2 S21 mutants induced an increase of late apoptosis.

In particular, eEF1A1-HIS S21A and S21D mutants induced mainly an increase of early apoptosis whereas eEF1A2-HIS S21A and S21D mutants induced an increase of late apoptosis.

Consequently, by analogy with the T17M RHO retinas, we analyzed the inflammatory markers and discovered that class I RHO mutants induced an increase in IL-1 β, thus suggesting that UPR and inflammatory activation occurred concomitantly in both the ADRP models.

In addition, these two mutants induce a constitutive β-arrestin recruitment.

While all 4 mutants induce a typical LT+ phenotype, RISP disruption additionally leads to an unusually perinuclear concentration of LysoTracker punctae, which was replicated by expression of RNAi against RISP (Fig. 4G).

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