Those variations have been discovered by scientific collaborations such as the International HapMap Project, which search for mutations of the genetic code called single-nucleotide polymorphisms, or SNPs, in blocks of DNA called haplotypes.
CCLE included around ~500 human cancer cell lines profiled for mutations of >1,600 genes, copy number variation of ~20,000 genes, expression profiling of ~20,000 genes, and pharmacological profiling of 24 compounds.
The results obtained from CGP were successively validated in the independent CCLE dataset, including around 500 human cancer cell lines profiled for mutations of >1,600 genes and pharmacological profiling of 24 compounds.
Prompted by these findings we have examined acute myeloid leukemia, non-Hodgkin's lymphoma, T-cell acute lymphocytic leukemia, B-cell acute lymphocytic leukemia and adult T-cell leukemia DNA for mutations of the FBXW7 gene.
This paper reports benchmarking of six protein stability calculators (POPMUSIC 2.1, I-Mutant 2.0, I-Mutant 3.0, CUPSAT, SDM, and mCSM) against 134 experimental stability changes for mutations of sperm-whale myoglobin.
All of these women were tested for mutations of factor V Leiden, methylenetetrahydrofolate reductase, and prothrombin gene; deficiencies of antithrombin-III, protein C, and protein S; and the presence of antiphospholipid antibodies and fasting homocysteine concentration.
The guidelines recommend performing a karyotype analysis in each couple and the screening test for mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) in one of the two partners.
In this article, we present an automated protocol for setting up alchemical free energy calculations for mutations of naturally occurring amino acids (except for proline) that allows an unprecedented, automated screening of large mutant libraries.
It should be noted that the ratio for mutations of M. tuberculosis isolated from macaques with latent infection increased drastically to 0.67 (Ford et al., 2011), indicating that oxidative DNA damage is a dominant source of mutation during both active and latent phases of M. tuberculosis.
We were therefore interested in learning if expression of one of the Notch targets, Hes1, could by-pass the need for mutations of Notch receptors.
Site directed mutagenesis of Fk3 makes the a4 promoter virtually insensitive to Foxi1 expression in contrast to the very limited effects on Foxi1 inducibility noted for mutations of Fk4 (Fig. 5A).
