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Research efforts on opioid receptor signalling in the past decade suggest that differential signalling pathways and downstream molecules preferentially mediate distinct pharmacological effects.
Spatiotemporal regulation of signaling pathways and downstream transcription factors controls GI epithelial morphogenesis during development to confer essential regional-specific epithelial structures and functions.
Identifying and characterizing these essential pathways and downstream gene sets is a clear future direction of this mouse model.
In conclusion, this study identified key molecular pathways and downstream target genes involved in the leptin-mediated weight loss.
In this study we have identified key molecular pathways and downstream genes which respond to leptin treatment and are involved in leptin-mediated weight loss.
Separating these processes is difficult because the same upstream signaling pathways and downstream effectors control both force generation and viscoelastic resistance [21], [22], [23], [24].
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These findings point to a model in which poly-synaptic circuit development reflects independent, highly stringent wiring of each parallel pathway and downstream station.
Measurement of molecular target status, pharmacokinetic (PK) parameters of drug exposure, and pharmacodynamic (PD) endpoints of drug effects on target, pathway, and downstream biological processes are extremely important.
This requires further analysis of mRNA and protein turnover, and post translational protein modifications such as phosphorylation, associated with components of the signal transduction pathway and downstream targets.
Though the JNK and NF-κB signaling pathways appear to cooperate in the control of Drosophila immune responses [19], the precise role of JNK pathway and downstream targets in host immune responses remains unclear.
Previous studies elucidated the GA signalling pathway and downstream factors.
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