Sentence examples for interference in the phosphorylation of from inspiring English sources

mTORC1 phosphorylation inhibits autophagy, while interference in the phosphorylation of this residue by Rapa stimulates autophagy induction.

We also explain that these results indicate that the phenotypes in foscrb Y10A embryos are due to the conformational distortion of the FERM-domain binding motif of Crb (as recently shown by Wei et al., 2015 J Biol Chem 290 11384), and not because of a putative interference with the phosphorylation of Crb in this tyrosine residue.

Based on our RNA interference data implicating DYRK1A in the phosphorylation of tau protein at multiple sites (Figure 1), we tested the high affinity DYRK1A inhibitor harmine for effects on tau.

On the contrary, depletion of hMena by specific RNA interference reduces the phosphorylation of HER3, p44/42 MAPK and AKT and inhibits both EGF and NRG1-mediated phosphorylation of HER2 and EGFR as well as cell proliferation.

Increased PAK1 phosphorylation was observed in HBMEC expressing cAc-Rac1 with a concomitant reduction in the phosphorylation of MLC.

Significant increase in the phosphorylation of c-Jun S63 was observed among other kinases.

Binding of growth factors activates mTOR signaling, which in turn leads to downstream phosphorylation of protein kinases, e.g., p70S6 kinase and lipid kinases in the phosphorylation of phosphoinositides.

However, proteins involved in the phosphorylation of MDA5 were not reported.

Thus, in theory, increasing concentrations of the interference peptide will decrease the phosphorylation of wild-type YB-1 and prevent it from binding to growth promoting/resistance genes.

In contrast to the phosphorylation of TAZ on serine or threonine, tyrosine phosphorylation also exists on TAZ.

Similar effect was observed in AMPK‐RNAi Drosophila, and we found that when RNA interference of AMPK was used in Drosophila, β‐GPA treatment failed to increase the phosphorylation of Atg1 in Drosophila (Fig.  5C).