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Consequently, more intense pressure mutation could result from the developing detonations.

In addition, our structural analyses illustrated that F1174V mutation could result in some important interactions, which represent the key characteristics of the ALK active conformation.

Although it is unclear how this mutation leads to TGMS, the following observations in other species suggest a logical pathway by which the RNZ m mutation could result in TGMS.

A mutation in a preferentially expressed allele would result in a dominant phenotype, whereas the same mutation could result in incomplete penetrance if the respective wild type allele showed preferred expression.

Very little myomesin staining could be detected in the hsp90α1 mutant embryos (Fig. 8D), suggesting that the hsp90a1 mutation could result in a dramatic disruption of M-line organization in skeletal muscles.

This mutation could result in less efficient capture of the rotating DNA segment, an increased lifetime of the covalent phosphotyrosyl intermediate (lower klig), and/or suboptimal positioning for strand ligation when high superhelical torque is present.

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Moreover, these mutations could result in the interaction of the mutated DLG3 with NEDD4 -2) while also disrupting the trafficking of the complex toward the synapse,, (Fig. 1).

Errors followed by reversals or absence of mutations could result in a descendant with the same phenotype as their ancestor.

Conversely, enz mutations could result in an increase in chromatophore cell death that would result in reduced numbers of cells.

Changes in the expression pattern and accumulation of new mutations could result in new functions for the duplicated gene copy.

These different ZF mutations could result in differential interaction with other editosome proteins which might affect their conformation, catalytic activities, and/or interaction with RNA substrates; they could also impair direct interactions between KREPA3 and RNA substrates in distinct ways.

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