Sentence examples for mutations we hypothesized from inspiring English sources

Since immunodominant CTL responses in acute infection have been identified as the major selection force driving the development of CTL escape mutations, we hypothesized that patient latent viruses should carry mutated epitopes which could not be recognized by immunodominant CTLs.

Finally, since error-prone repair or TLS of oxidized DNA lesions will contribute to mutations, we hypothesized that MutS and DinB play opposing roles in P. aeruginosa pathoadaptation.

Because rapamycin can alter T cell function and prevent the development of NNK-induced lung tumors that are associated with K-Ras mutations, we hypothesized that modulation of immune function might be an important determinant of lung tumorigenesis.

Inasmuch as MutS acts to prevent mutations, we hypothesized that MutS function might contribute to accurate repair of ROS-damaged DNA, and that in the absence of MutS, P. aeruginosa would be impaired for coping with these lesions, possibly explaining the reduced virulence of this strain in a murine model [28], [43].

To model kinase inactivating mutations, we hypothesized that mutations that alter catalytically essential residues (e.g., residues mediating ATP binding, Mg2+ coordination or phospho-transfer, as defined in Zeqiraj and van Aalten, 2010 and Table S5) could lead to kinase inactivation.

Because driver mutations by definition are associated with a greater number of cancer phenotypes compared to other mutations, we hypothesized that driver mutations could more easily be identified once the genotype-phenotype correlations are detected across tumor samples.

Given that self-cleavage can be either slowed or enhanced by mutations, we hypothesize that the LexA cleavage rate has been selected for to allow for proper activation of the SOS pathway and that LexA may serve as a rheostat for evolution under stress.

Based on our functional studies on β-MHC mutations, we hypothesize that the mechanism responsible for the severe phenotype in patients with a large fraction of mutated β-myosin is a functional imbalance among individual cardiomyocytes because of unequal expression of the mutant protein from cell to cell [ 15].

DOI: http://dx.doi.org/10.7554/eLife.00825.013 Given that a substantial number of MYBL2-low cases lacked either a 20q deletion or gene-specific inactivating mutation, we hypothesized that additional mechanisms of MYBL2 downregulation exist in MDS.

Having demonstrated that BD-L was enriched in BRCA1 mutation carriers, we hypothesized that breast cancer cell lines with elevated BD-L values may exhibit increased sensitivity to therapeutic agents that target a dysfunctional BRCA1-associated pathway.

In the light of the few reports of EB causing mutations in livestock we hypothesized that a causative variant might affect one of the known EB candidate genes.