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In addition, amongst the 39 genes that were only mutated once, 12 (31%) of the mutations were nonsense mutations.
ACE2 was mutated in eight evolved clones; six of these mutations were nonsense mutations scattered through the open reading frame.
UBR1 was mutated in 6 of the 12 clones; four mutations were nonsense mutations, strongly suggesting that the remaining two are also a loss of function mutations.
Other mutations were nonsense or frame-shifts.
Interestingly, three of the six BRCA2 mutations were nonsense and three were novel.
Only a small portion of these mutations were nonsense mutations (115, 5.1%), which likely truncate protein sequences.
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As many as 90% of all mutations are nonsense mutations, causing a truncated polypeptide product.
A large number of KMT2D and KDM6A mutations are nonsense mutations that produce aberrant PTCs that are potentially deleterious.
Most of the remaining mutations are nonsense mutations that result in the production of truncated forms of Fbxw7.
Four of the six mutations are nonsense mutations, suggesting that we selected for inactivation of this protein.
However, most of the identified XRCC4 mutations are nonsense or frameshift changes, predicting the synthesis of truncated proteins.
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