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This fact is consistent with our class III mutants, where we found that a >250 molar excess of K+ was unable to suppress hygromycin B sensitivity.

With no firmly established role for Foxc1 in regulating cell proliferation, one intriguing possibility comes from profiling data on microvessels isolated from pericyte conditional Foxc1 mutants where we observed altered expression of pericyte-expressed proteoglycans asporin and glypican-3.

The assay also allowed us to look at membrane "binding/insertion" of our different epsin mutants where we could show that the L6W mutant bound more tightly than WT protein.

Next we investigated Fmi trafficking in fz, stbm double mutants, where we predict that Fmi would be less stabilized at the plasma membrane and rates of endocytic trafficking would increase.

Of the mutants where we investigated the amino acid substrate specificity (Table 2), p.Arg233His, p.Cys359Phe, p.Phe375Leu, and p.Gly414Arg are mutations structurally positioned to affect active-site residues (Fig. 4), and they only showed a moderately reduced solubility and thermal stability (Table 3).

Similar(55)

A case in point for (i) is the Sec24b mutant, where we found the surprising link between Sec24b-dependent COPII-coated endoplasmic reticulum to Golgi protein transport, Vangl2 trafficking and PCP[12].

We produced recombinant FL-MMP-11 mutant where we replaced GI by AV (FL-MMP-11/AV) and tested the activity of Cat-MMP-14 on this mutant.

Interestingly in blu-/ mutant, where we observe Ntf3 overexpression and RCGs axons are expanded, the fraction of presynaptic boutons associated with mitochondria was unaffected.

The lone exception is the spt16 -K579E mutant where we detected a stronger decrease in the occupancy of the mutant protein expressed from this allele than expected based on a relatively modest decrease in histone H3 occupancy.

Using ChIP, we measured the occupancy of Tup1p in the rpd3 hdoubleuble mutant where we had previously shown histone hyperacetylation across the FLO1 promoter region and partial FLO1 de-repression.

Interestingly in blu-/ mutant, where we observed Ntf3 overexpression and RCGs axons are expanded, the fraction of presynaptic clusters (visualized by synaptophysin-GFP) associated with mitochondria was unaffected, suggesting that Ntf3 does not have an impact on mitochondria association with synapses.

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