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MacCarthy, T. et al. V-region mutation in vitro, in vivo, and in silico reveal the importance of the enzymatic properties of AID and the sequence environment.
To elucidate the functional significance and consequence of the LRP5 G171V mutation in vitro, we took a structure-based approach to design 15 specific LRP5 point mutations.
Finally, we explored the subcellular mechanism of the mutation in vitro.
In addition, the resin composite co-monomer, TEGDMA, can cause gene mutation in vitro [5 7].
Indeed, we recently demonstrated that this inhibitor effectively targets wild type and mutant BCR-ABL positive cells, including the T315I mutation, in vitro [26] and in vivo [31].
Moreover, we find that the A66W mutation has a unique, severely negative impact on development, which may be explained by enhancement of tubulation and vesiculation induced by this mutation in vitro [8].
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We also confirmed that R299Q was a loss-of-function mutation using an in vitro reporter assay system.
This sub-discipline was galvanized by the invention of DNA shuffling, a procedure that randomly recombines point mutations in vitro.
We functionally characterized mutations in vitro and studied immune profiles and regulatory T (Treg) cells.
On the other hand, concentrations of both inhibitors that induce mutations in vitro are well above 1.0 µM [41], [56].
The lack of anti-bacterial activity demonstrated with Crohn's-associated Nod2 mutations in vitro, supports the hypothesis that a deficiency in direct bacterial killing contributes to the association of Nod2 polymorphisms with the disease.
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