Sentence examples for mutants to regulate from inspiring English sources

While the differing capabilities of VHL disease-associated mutants to regulate HIF have been explored [20], [21], [23] [25], the mechanism of retained HIF regulation and the link between differing levels of HIF regulation and the clinical spectrum observed in VHL disease is not yet fully understood.

Analysis of the ability of these mutants to regulate the activity of calcium and potassium channels, adenylyl cyclase 2, phospholipase C-β2, and β-adrenergic receptor kinase revealed the Gβ residues required for activation of each effector and provides evidence for partially overlapping domains on Gβ for regulation of these effectors.

Thus, the inability of these mutants to regulate their adhesive interactions likely results in their inability to complete the entry process.

Thus, the effect of the Lis1 mutations on dynein binding correlates with the ability of the Lis1 mutants to regulate dynein at the single-molecule level.

We have here revealed a direct transforming potential of BIRC2 and BIRC3 mutants that is, at least in part, unrelated to the ability of these mutants to regulate NF-κB signaling.

We developed a system to influence protein abundance and activity genetically, which can be used to create conditional mutants, to regulate the fate of single protein domains or to design artificial regulatory circuits.

To study the ability of RCC-associated mutant pVHL to regulate HIF in 786-0 cells, the hypoxia mimetic cobalt chloride (CoCl2) was used to simulate hypoxic conditions.

Surprising, it was recently found that a P53 point mutant unable to induce apoptosis, cell-cycle arrest, or senescence retained the ability to prevent tumorigenesis, presumably as a result of the ability of the mutant protein to regulate energy metabolism and production of reactive oxygen species [ 48].

Although our previous studies suggested that Crc and Lp mutants interact genetically to regulate cardiac development, and Lp mutants have significant myocardial disorganization similar to that seen when Scrib is lost from the myocardium, the current study suggests that this is unlikely to be a consequence of a physical interaction between the two proteins.

Importantly, NKX2-5 mutants were shown to regulate the expression of these off-target genes, which together could be viewed as a "mutation-acquired gene regulatory network".

We conclude that Pif1, like Exo1, is important for ssDNA generation after telomere uncapping in cdc13-1 mutands appearsears to regulate a nuclease activity, which functions in parallel to Exo1 at chromosome ends.