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In parallel – and this can be seen as an internal validation of our hypothesis – we observed that genes of the translation machinery, expected to be expressed at a high level (and hence under a "mutator" pressure) were indeed mutated, but that the corresponding mutations were usually of the synonymous class.

In imatinib-resistant lesions, secondary KIT mutations were usually acquired in addition to primary KIT mutations [10 12].

Since drug resistance mutations were usually associated with a negative influence on RC, as previous results showed, the initial correlations between RC and the clinical markers could not be observed at the follow-up points.

Indeed, most frequently, TP53 mutations were shown to be associated with prognosis in Asian populations infected by HBV, 44 46 whereas in a series of patients with mixed aetiologies, TP53 mutations were usually not an independent prognostic marker.

Recent studies showed that recurrent loss-of-function mutations in the dominant negative helix loop helix protein ID3 gene occurred in 34 68% of BL. 70– 72 ID3 mutations were usually biallelic, and nearly all alterations in ID3 affected the highly conserved HLH domain, resulting in impaired interaction with binding partner proteins (Fig. 1).

Targeted mutagenesis of many zinc transporters in mice have not yet been performed and for those that have been targeted, mutations were usually generated ubiquitously instead of in a tissue-specific manner, making analysis of their specific role in dietary zinc absorption difficult.

Similar(54)

P element insertion screens allow easier identification of mutated genes, but P element mutations are usually not nulls, and on average have weaker embryonic phenotypes than EMS mutations in the same genes.

The mtDNA point mutations are usually heteroplasmic and maternally inherited.

These mutations are usually frameshift and hemizygous, suggesting it may be a tumor suppressor, like ARID1A.

These mitochondrial DNA mutations are usually detected by conventional polymerase chain reaction followed by restriction enzyme digestion and gel electrophoresis.

For example, while disadvantageous mutations are usually eliminated quickly in large populations, new advantageous mutations are almost as vulnerable to loss through genetic drift as are neutral mutations.

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