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PSA signals through TLR2 and initiates the production of cytokines modulating Th1/Th2 balance (activation of NF- κB, regulation of TNF α, IL-12 production).
The interaction of herpes virus entry mediator with BTLA induces bidirectional signaling pathways that balance activation and inhibition to regulate T-lymphocyte activation [ 3].
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If the intensity and the duration of the effort required to perform the task are balanced, activation will take place in an optimum area, which makes the subject efficient.
FcγRs are responsible for balancing activation (FcγRI, FcγRIIa and FcγRIIIa) and inhibitory signals (FcγRIIb) of the immune system with the ability of both activating and inhibiting the IgG mediated effector stimulation [1], [19].
Regulation of the immune system follows an interplay between molecules and their receptors by balancing activation and inhibition in a timely manner.
Balanced activation of MR and GR is considered essential for efficient regulation of the stress response which is crucial for the maintenance of homeostasis and mental health (Oitzl et al. 2010).
Since the interplay between kinases and phosphatases balances activation and inactivation of proteins and with it the cross-talk between signaling cascades and metabolic pathways [ 33], measurement of transcriptional activity of kinase-encoding genes is important for understanding drought-response homoeostasis.
The integration of Ras-MAPK and TGFβ pathways can occur via balanced activation of both canonical and noncanonical TGFβ pathways by TGFβ alone, through simultaneous stimulation of TGFβ and ligands of other signaling pathways that modulate the activity of Ras-MAPK, or through crosstalk via interactions between the intracellular effector proteins distinct to each of the two pathways.
The pattern of activations in each network then represents a (perhaps locally) optimal configuration that balances activations in response to weights between connected nodes.
Significantly greater proportions of the Vδ1+ and Vδ2+ γδ T cell subsets were activated in patients with active BD; however, the balance of activation favored Vδ1+ T cells [ 31].
There are multiple pathophysiologic mechanisms underlying abnormalities in circadian BP, most importantly abnormalities in sympathetic nervous system activity, salt and volume balance, and activation of the renin angiotensin system.
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