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Intracellular cAMP levels are the result of a balance between synthesis, which is regulated by G-protein-coupled receptors that stimulate (via Gs) or inhibit (via Gi) adenylyl cyclase (AC), and degradation, which occurs via cyclic nucleotide phosphodiesterase (PDE).
Activation of pathways other than TLR was inadequate to stimulate, via cross-talk mechanisms through molecular hubs, the production of proinflammatory cytokines typical of a TLR response.
The induction of miR-155, miR-146a and miR-146b has been shown previously in response to viral and bacterial mimics that stimulate via a variety of TLRs [6], [7], [8], [10], [11], however this is the first study to look at their induction by fungal ligands.
In the present study, our data showed that FTY720 is able to stimulate, via the inhibitory G proteins, Pak1 and Akt autophosphorylation and activities and trigger NO release through eNOS.
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CD83 expression on B cells reached a maximum at six hours post stimulation in cultures stimulated via BCR- or TLR-engagement.
Briefly, B cells were stimulated via NIH3T3 stimulator cells stably expressing human CD154.
Rats, stimulated via the sciatic nerve, were subjected to 3x 10min (1Hz) stimulation bouts with 30min rest between or a single bout (2Hz) to 50% fatigue.
These actions of maggot secretions on the differentiation of macrophages are not limited to stimulation via TLR-4 as similar effects were observed when stimulated via the TLR-2 pathway.
Neurotransmitters in the brain are stimulated via the opening of specific ion channels to allow sodium ions to flow into the nerve cell.
The target areas are stimulated via the electrodes which are connected to a battery-powered pacemaker surgically placed under the patient's collar bone.
The detectors are coupled to a fiber optic delivery system and OSL from the detector is stimulated via the optical fiber cable using light from a Nd YAG laser.
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