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This finding supports the notion that the mutation was obtained upon the divergence of cluster P2.
Collectively, our experimental results are consistent with the notion that the mutation in the aromatic finger compromises autophagy through crippled membrane association by Beclin 1, rather than through reduced interactions with other cellular proteins.
Our clinical data strongly support the notion that the mutation of TP53 in type I tumours converts them to an aggressive tumour type, reflected in the poor survival of patients whose type I tumours exhibited frequent strong p53 nuclear immunoreactivity.
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These data are consistent with the notion that the T790M mutation, when combined with activating EGFR kinase domain mutations, confers enhanced catalytic phosphorylating activity, as shown by others using insect cells infected with baculovirus expressing various EGFR intracellular domain constructs [19].
The absence of the oncogenic mutations commonly linked to the activation of the ERK pathway in melanomas, the strong association of the Grey mutation with the melanoma predisposition [ 17] and the notion that the Grey mutation has an effect throughout melanocyte development [ 18], prompted us to test if the ERK pathway was already activated at the level of normal skin melanocytes in Grey horses.
Co-sedimentation experiments also supported this notion that the K1647D/K1650D mutation interferes with co-pelleting of the MyTH4 FERM domain with microtubules but the F2002K mutation causes no interference.
We also observed that the epidermal cells of the 2nd leaf sheath in HNIL(H143) were significantly longer than those in HNIL(M23) after uniconazole treatment (Fig. 3c), supporting the notion that the el1 mutation (type 2) in H143 leads to an enhanced GA signaling response, even in the absence of GA.
The synaptic levels of these proteins were unchanged (Fig. 7), further supporting the notion that the YG mutation does not affect APP maturation and trafficking and that APP may not be a regulator of fast anterograde axonal transport.
These data support the notion that the sply mutation suppresses dys phenotypes by increasing levels of phosphorylated sphingoid bases (Pantoja et al., 2013).
The analysis of molecular dynamics trajectory presented in this paper supports the notion that the p.Cys169Tyr mutation hinders the docking of Cx26 hemichannels by altering protein structure in the extracellular domain.
Our in vitro and in vivo data also support the notion that the GREM2 Q76E mutation generates a hypermorphic allele and a pathogenic genetic variant that increases the risk of AF.
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