Sentence examples for mutations of the three from inspiring English sources

Nonetheless, simultaneous mutations of the three LRR-RKs genes (pxy-3 with pxl1 and pxl2) generated an enhanced vascular phenotype observed in pxy-3 plants with flatter vascular bundles and a less clear distinction between xylem and phloem.

Furthermore, a role of PXL2 in vascular tissue development is also in line with the genetic data showing that simultaneous mutations of the three LRR-RKs genes (pxy-3 with pxl1 and pxl2) generate a more striking vascular phenotype as compared to the pxy-3 plants.

To further characterize the function of the base excision repair pathway in plants, we have located and combined insertion mutations of the three abasic endonuclease genes.

Importantly, mutations of the three intragenic AP-1 sites decrease RNAPII in vivo recruitment to the viral promoter, supporting the notion that these sites are important for HIV-1 transcriptional activity.

Importantly, mutations of the three intragenic AP-1 sites led to a decreased in vivo recruitment of RNA polymerase II to the viral promoter, strongly supporting that the deleterious effect of these mutations on viral replication occurs, at least partly, at the transcriptional level.

PIK3R1 mutations as well as combined mutations of the three genes studied were also found to be mutually exclusive with PTEN underexpression (p = 0.00016).

Mutations of the two Cys residues can significantly impair the binding ability of hCutC with Cu(I).

For example, mutations of the four positively charged residues, R1639G, R1642S, R1645Q, and R1648C, are present in the domain IV S4 segment (Table 2), suggesting that these EIEE6 mutations may alter the voltage sensing behavior of the channel.

Somatic mutations of the two genes coding for the histone acetyltransferase genes, CREEBP and EP300 have been identified as a pathogenetic mechanism shared by common forms of B-cell non-Hodgkińs lymphomas.

As shown in Figure 3B, FBS and WY-14643 efficiently induced CYP1A1 promoter transactivation (2.5-fold) while the mutation of one PPRE site alone slightly reduced luciferase activity, and the mutations of the two PPRE sites abrogated it.

In contrast, mutations of the miR-128 and 27a/b binding nucleotides 14 and 236 of the 3'-UTR relieved the miR-mediated repression of luciferase activity.