We find that the more fusogenic variants induce an unaligned lipid phase component and a large degree of phase separation as observed in 31P 2D spectra.
One of the variants induced a frame-shift mutation that could lead to nonsense-mediated mRNA decay, a ubiquitous cellular mechanism that eliminates mRNA containing a premature termination codon.
Each protein variant is composed of one or more exons, each of which corresponds to a contiguous stretch of nucleotides within U. Therefore each protein variant i∈{1,…, n}, where n is the total number of variants, induces a subset S i of U, and the union of all S i ∈{1,…, n }= U. Our goal was to find the minimum number of sets within { S1,…, S n } that maximally cover U.
Taken together, these results suggest that A30P and E46K, as opposed to either Wt α-Syn or the A53T variant, induce a pro-inflammatory response in glia.
Hence, the MICA-129Met variant induced a stronger down-regulation of NKG2D than the MICA-129Val variant.
The Pro143Ala variant induces a transformation of the shape of helix α1 compared to HTRA2 (1LCY) (Fig. 3a, red circle indicates the helix α1).
Importantly, the MICA-129Met variant induced a stronger down-regulation of NKG2D on NK cells and even more on CD8+ T cells than the MICA-129Val isoform.
On the other site, the MICA-129Met variant induced a faster and stronger down-regulation of NKG2D on NK and cytotoxic T cells than the MICA-129Val isoform.
Consistent with some of the in vitro binding data, the R1838A variant induces a small but significant degree of apical constriction; a 22% decrease in apical area relative to non-transfected cells (Fig. 4B,D).
CrkII localization within pedestals was shown to be dependent on the phosphorylation of Y474 of Tir, although it should be noted that the Y474F variant induces a very limited number of pedestals.
