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Various diseases have been attributed to mutations of TRP channels.
As we have seen, all of these substitutions, except for the highly variable sites 44 and 89 have been attributed to mutations that took place solely in the anthropoid lineage long after anthropoid divergence from strepsirrhines such as O. garnettii.
Unlike well-defined oncogenic (e.g. c-kit) or tumour suppressor pathways (e.g. p53), no human cancers have been attributed to mutations or loss of the core signalling components of the Hippo pathway[3].
Approximately 50% of FAD cases have been attributed to mutations in three genes, amyloid precursor protein (APP) [1], presenilin-1 (PSEN1) [2] or presenilin-2 (PSEN2) [3].
Notably, over 20 muscle related diseases have been attributed to mutations in sarcomeric proteins, including Z-disc associated proteins, further underlining their importance [106].
While HIV-1 can escape therapeutic interfering RNAs, this has been attributed to mutations that occur in or near the target region and not to generalized inhibition of RNAi [28], [29].
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By genetic analyses, this could be attributed to mutations either in the GLUT transporter sequence or in the genome of the yeast host.
Such three low-Cd mutants were attributed to mutations of OsNRAMP5 responsible for Cd transport in rice by sequence analysis (Ishikawa et al. 2012).
Most of autosomal dominant familial AD can be attributed to mutations in one of three genes: those encoding amyloid precursor protein (APP) and presenilins 1 and 2. Most mutations in the APP and presenilin genes increase the production of a small protein called Aβ42, which is the main component of senile plaques.
Continuous proliferation of cells in serum-free medium could be attributed to mutations of key genes (e.g., K-Ras).
CF is attributed to mutations in the CFTR gene, coding for the Cystic Fibrosis Transmembrane Regulator, a multifunctional transmembrane chloride channel [4].
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