Words similar to guanine-nucleotide
Example sentences for: guanine-nucleotide
How can you use “guanine-nucleotide” in a sentence? Here are some example sentences to help you improve your vocabulary:
The A326S mutation of α i1 and A366S mutation of α s (cognate to the α i2 A327S used in this study) were shown to cause greatly decreased affinity for GDP [ 9 10 ] . Defective binding of GDP leads to more Gα in the empty state (no bound guanine-nucleotide), and this form of Gα is rapidly denatured in vitro , as shown for α s A366S and α i1 A326S [ 9 10 ] . Moreover, α s A366S was demonstrated to undergo rapid degradation (t 1/2 < 1 h) in stably transfected cells [ 9 ] . The same mutation in α t has also been shown to greatly decrease guanine-nucleotide binding [ 5 22 ] . Additional amino acids in the critical β6-α5 loop are important for maintaining Gα integrity [ 7 ] .
A recent study identified a number of α5 helix residues in α t that when changed to alanines increased rates of guanine-nucleotide exchange ( i.e., decreased affinity for guanine-nucleotides) [ 5 ] . Individual mutation of amino acids in α t , cognate to T330, N332, V333, F337 in α i2 (Figure 1), increased nucleotide exchange rates [ 5 ] . Two of these critical amino acids, N332 and V333 in α i2 , are in fact the first two amino acids that are replaced by the novel splicing in sα i2 (Figure 1).
The C-terminal 30 amino acids of Gα consist of the β6-α5 loop, followed by the α5 helix and finally several amino acids of flexible structure (Figure 1) [ 19 20 21 ] . The β6-α5 loop stabilizes the guanine ring of bound GDP or GTP, and mutations in this region affect guanine-nucleotide binding.
The following results support this hypothesis: 1) sα i2 and α i2 are equally labeled by a pulse of 3H-myristate, although much less sα i2 protein is detected; 2) sα i2 displays a propensity to localize to potential aggresome-like structures, and this localization is greatly enhanced by proteasome inhibitor treatment; 3) the α i2 A327S mutant, previously shown to be unstable and defective in guanine-nucleotide binding, shows a similar pattern of subcellular localization ( i.e., intracellular membranes rather than PM); 4) βγ over-expression increases expression of sα i2 and promotes PM localization of sα i2 and α i2 A327S, but βγ co-expression does not prevent sα i2 localization to potential aggresome-like structures when cells are treated with proteasome inhibitors; and 5) pulse-chase analysis indicates that sα i2 is rapidly degraded.
Unfortunately, initial attempts to directly show a defect in guanine-nucleotide binding by sα i2 , using a GTPγ S-dependent trypsin protection assay [ 23 ] , were unsuccessful due, at least in part, to the inability to solubilize expressed sα i2 from membranes using a mild detergent ( e.g., lubrol/polyoxyethylene 10-lauryl ether).
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