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To analyse the activation of HER2 and its downstream related phosphoinositide-3 kinase/protein kinase B (PI3K/AKT) and mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK1/2) signalling cascades or to the mammalian target of rapamycin protein (mTOR) signalling pathway, we performed Western blotting and immunohistochemical analysis of each individual animal tumour.
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In contrast, in our study we analysed the activation of the GPHR TMDs based on the TMD_In and TMD_Ac structures of the three receptors.
Alk4* expression and function were tested by analysing the activation of Smad2 (P-Smad2) after Dox or SB treatment in western blots.
We analysed the activation of cellular markers that are characteristic of apoptosis by immunoblotting.
For the analyses, the activation of the reading condition could be subtracted from the activation of the other conditions.
To further verify the importance of the CWI pathway for ccw12Δ cells, we analysed the activation of Slt2p.
In order to investigate the molecular pathways responsible for the reduced muscle growth, we analysed the activation of the ubiquitin proteasome and the autophagy-lysosome systems.
To assess whether any other caspases compensated for the loss of caspase-7, we analysed the activation of the effector caspase, caspase-3.
To determine if WLS also regulates endogenous WNT/β-catenin signalling, we analysed the activation of the BAR-luciferase reporter in A375 cells transfected with various siRNAs.
Since the sensitisation to apoptosis induction after combined exposure to TRAIL and IR may be due to the simultaneous activation of the caspase-8 and -9 pathways, we next analysed the activation of these distinct apoptosis pathways in clearCa-22.
Considering the pivotal role of caspases in the initiation and execution of apoptosis (Thornberry and Lazebnik, 1998), we next analysed the activation of caspase-3, -8 and -9 following CDDP treatment of NCCIT cells.
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