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There has been great debate about which sites and how many are required for deactivation of rhodopsin.
Analysis of Grk1-KO mice demonstrated that GRK1-mediated light-dependent phosphorylation is required for deactivation of activated rhodopsin, and absence of GRK1 leads to photosensitization of the rods and induces apoptotic death (Chen et al., 1999).
Furthermore, the amount of catalase required for deactivation of silica per unit area of particle surface is lower for fumed silica particles and calcined crystalline particles than for uncalcined, crystalline silica, suggesting a correlation between the concentration of OH groups at the silica particle surface and its potential for generation of H2O2.
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In zebrafish melanopsin, we conclude that sites 381, S338, and S394 are required for rapid deactivation.
Ptc2 and Ptc3 were not required for Rad53 deactivation and dephosphorylation following genotoxic stress in S-phase via hydroxyurea [ 123].
Pph3 was not required for Rad53 dephosphorylation and deactivation following replication stress.
Thus, distinct phosphatases appear to be required for the dephosphorylation and deactivation of Rad53 following various DNA damages in yeast and the phosphatase required for recovery from replication stress has not yet been identified.
A systematic study of catalyst deactivation is required for the development of a coke resistant and sulfur tolerant catalyst for diesel fuel reforming systems to be used in conjunction with the solid oxide fuel cell (SOFC).
The results obtained suggest that the properties required for a best-performing catalyst (maximum conversion and lowest deactivation rate) are different for these two alkenes.
This indicates PI3K is required for Sal B-induced Akt activation and c-Raf deactivation.
Moreover, fluvastatin treatments simultaneously increase the expression of the dCK, the enzyme required for the activation of gemcitabine, and reduce the 5′-NT, responsible for deactivation of gemcitabine, suggesting a possible additional role of these enzymes in the enhanced cytotoxic activity of gemcitabine in the combined treatment.
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