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Clearly, as yet unidentified additional mutations contributed to the small plaque phenotype of Yar 46-2 (D67G).
Among 13 patients with drug resistance, 5 (38%) had mutations contributed to only NRTI resistance; 1 (8%) had mutations contributed to only NNRTI resistance; and 7 (54%) patients had mutations contributed to both NRTI and NNRTI resistance.
For some time it was not known whether these mutations contributed to the ageing phenotype or whether these changes were just a consequence of the normal ageing process.
However, it was not clear how these mutations contributed to the ability of the bacteria in this population to use citrate.
To assess whether and to what extent these mutations contributed to butanol tolerance, the evolved strain IMS0344 was crossed with a Matα ura3Δ strain (IMK439) isogenic to the ancestor strain CEN.PK113-7D CEN.PK113-7D
This is consistent with the very low rate of rescue in 0.2-mL populations and the c. 50% probability in 1.5-mL populations in experiment 2, although we cannot exclude that de novo mutations contributed to rescues.
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Moreover, endothelin-1 upregulated by BMPR2 mutations contributes to PH pathogenesis (Star et al., 2013).
In human, NaV channels are therapeutic targets as their mutations contribute to many diseases.
Oncogenic IDH1 and IDH2 mutations contribute to cancer via production of R-2-hydroxyglutarate (2-HG).
In cancer patients, tumor gene mutations contribute to drug resistance and treatment failure.
These two mutations contribute to the aberrant PML-RARA SUMOylation and NB formation (Goto et al., 2011).
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