Sentence examples for most mutations lead from inspiring English sources

Most mutations lead to non-functional proteins.

This is most obvious in Werner syndrome, where most mutations lead to truncation of the protein; Bloom syndrome is also most commonly the result of truncation, although loss-of-function missense mutations have been reported [ 7].

Most mutations lead to premature stop codons, either directly as a result of nonsense mutations or indirectly through a shift in the normal reading frame by splice-site mutations or small insertions and deletions, thereby inducing the degradation of mutant RNA by nonsense-mediated decay - although other mechanisms have been observed [ 22, 36, 37].

In the soluble fraction, most mutations lead to a greater proportion of high-molecular-weight heterotrimers (Fig.  5H; Col4a1 +/G658D is used as a representative example) with the exceptions of Col4a1 +/G1344D and Col4a1 +/S1582P, which had a greater proportion of monomers.

Much as Riedl had noted that at an organismal level most mutations would lead to deleterious, unviable phenotypes, a similar observation has been made at the level of gene regulatory networks by Davidson and Erwin (2006, 2010) and Erwin and Davidson (2009).

Most proteins show an ω well below 1, since most mutations that lead to amino acid substitutions decrease fitness and hence are unlikely to become fixed between species (purifying selection).

Most FERMT1 mutations lead to premature termination codons and absence of kindlin-1.

Most OCA IA mutations lead to misfolded tyrosinase which is retained in the ER by the quality control (ERQC) and subjected to degradation by the ERAD pathway [18], [19].

This is consistent with the finding that most (86%) mutations lead to premature termination of the protein (Wicking et al, 1997; Fujii et al, 2003).

On an individual basis, it was striking that most single mutations led to only modest and non-significant decreases in the amplitude of the T cell response.

Most PTCH1 germinal mutations lead to premature stop codon [8], and in BCCs, are accompanied by somatic mutations or loss of heterozygosity (LOH) at the PTCH1 locus (9q22.3) [9], [10], as expected for a tumor suppressor gene [11].