Sentence examples for mutation we examined from inspiring English sources

In order to identify any biological consequence of the FYVE-CENT R1945Q mutation, we examined the phenotype of mutant cells by performing immunofluorescence microscopy using the HCC-1954 and HCC-1395 breast cancer cells.

To test whether loss of dCREB2 functions causes similar changes in energy stores as the TORC mutation, we examined glycogen and lipid levels in flies with a null mutation in dCREB2, a Drosophila homolog of mammalian CREB/CREM [13].

To gain insight into the nature of this separase mutation, we examined meiocytes of rsw4 exposed to the restrictive temperature and compared them to the previous results with RNAi.

To confirm the lncRNA selectivity of the F266A mutation, we examined its effects on MLL complex structure and catalytic activity in vitro.

To probe the properties of the expanded population in mutant glands with a Gal4 driver, whose expression is not downregulated by the effects of the mutation, we examined the expression of the 76B>Gal4.

To get some idea of the distance between the transposon-encoded Tetr marker and the beneficial mutation, we examined the co-transduction of the resistance marker and increased cell size, using REL10247 as the donor and the ancestor as the recipient.

Lastly, to determine whether 1, 9 PA can also sensitize cancer cells with naturally occurring Ras mutations, we examined the effect of the combination of 1, 9 PA and cetuximab on GEO colorectal cancer cells, which are known to have mutated Ras [31].

To test whether the T2/OncZ system is effective at producing genome-wide somatic insertional mutations, we examined the extent of re-integration following injection of SB11 mRNA into 1-cell stage embryos that had either the Tg(T2/OncZ, ß-actin:RFP is6 (∼500 copies) or Tg(T2/OncZ, ß-actin:RFP is7 (∼70 copies) concatemer (Fig. 3 A, Table 2, Experiments 1 and 2).

To identify the source of DSBs caused by Nde1 mutations, we examined their occurrence with respect to the cell cycle.

To search for spontaneous mutations, we examined the sequences throughout the genome for base substitution mutations and did not identify any sequences that differed from both parental sequences.

To determine if both signatures identify tumors with TP53 mutations, we examined the TCGA breast cohort and extracted the gene expression data (RNA-seq) for each gene comprising the signature as well as TP53 mutation status.