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This suggests that mGluR5 may trigger protein synthesis to enable persistency of synaptic plasticity.
This is of great relative interest to this contest because, as shown in our series, it is possible to argue that H-I insult occurring during CPB phase may trigger protein's release due to "multiorgan" stress of whom CNS constitutes the majority of the total protein's amount [ 3, 4, 36].
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However, our results suggest that high levels of SOD protein may trigger an unfolded protein response that contributes to the increase in life span.
Subtle changes in the molecular shape of the protein may trigger insolubility of the protein, loss of biological function, or increased immunogenicity due to the uncovering of antigenic portions of the molecule that would normally be hidden from the immune system [ 1,46 48].
Scientists have shown how a single protein may trigger autistic spectrum disorders by stopping effective communication between brain cells.
Although variable and constant regions within the SRLV SU protein may trigger the production of neutralizing antibodies [ 31], the main sites/epitopes involved in this process have not been identified.
In addition, the Fc-portion of the TACI-Ig fusion protein may trigger signaling via Fc-receptor (FcR -activation on myeloid cells or clearance oFcR -activationB-cell subsets by alternative mechanisms than death upon BAFF depletion.
For example, protein phosphorylation may trigger substrate degradation by proteolytic enzymes, direct intracellular protein sorting or drive the assembly/disassembly of active complexes in signaling, transcription, translation, cell division and organelle biogenesis.
In this scenario, TIF1β would interact with viral proteins and the putative viral-self protein complex may trigger autoantibodies to TIF1β, similar to the induction of anti-p53 by a complex of viral simian virus 40 T protein and self p53 protein [ 37].
These chemically modified proteins may trigger T cell-mediated immune reactions and lead to ACD [3].
ERK-mediated changes in transcription factor activity may trigger the synthesis of proteins that underlie the maintenance of L-LTP.
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