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Their actions are mediated via binding to PRL receptor (PRLR), highly expressed in brown adipose tissue (BAT), yet their impact on adipocyte function and metabolism remains unclear.
The neuropeptide α-MSH has been shown to exert multiple anti-inflammatory and immunomodulatory effects whereas in particular the immunomodulatory effects are mediated via binding to MC-1R [42].
In humans and rodents, these actions are mediated via binding of lactogens to the prolactin receptor (PRLR), a class I cytokine receptor linked to activation of the JAK/STAT signaling pathway [2].
The majority of TCDD effects are mediated via binding and activation of the intracellular aryl hydrocarbon receptor (AhR), as demonstrated by the loss of responsiveness to TCDD in AhR knockout mice [5].
Normally, endothelial cells have higher-than-average tolerance for the cytolytic attack of CD8+ T-cells, and this down-regulation is mediated via binding of programmed death 1 –receptor (PD-1) on CTLs to the ligand PD-L1/L2 expressed on endothelial cells.
The activity of somatostatin is mediated via binding to specific cell surface receptors.
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Initial leukocyte rolling is mediated by E- and P-selectin whereas firm adhesion to the vascular wall is mediated via integrin binding with intercellular adhesion molecule-1 (ICAM-1) and VCAM-1, with the latter more important in initiation of atherosclerosis [6,53].
In summary, we demonstrated that both rATG and alemtuzumab induce rapid apoptosis in NK cells and a strong induction of inflammatory cytokines, which is exclusively mediated via the binding of the IgG1 Fc-part to the low-affinity receptor for IgG, CD16 (FcγRIII).
Hh signalling is mediated via ligand binding (Sonic, Indian and Desert hedgehog) to the receptor Ptch.
The original murine CD3 mAb, OKT3, potently reversed allograft rejection but caused a profound cytokine release syndrome on initial dosing, mediated via FcγR binding [ 40].
Although c-myc is considered to be an E2-regulated early response gene, its promoter does not contain a consensus ERE but its E2 responsiveness is reported to be mediated via Sp1 binding (Dubik and Shiu, 1992).
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mediated via head-to-head
mediated via parkin
mediated via caveolae
mediated via inhibition
mediated via chemokine
mediated via membrane
mediated via apoptosis
mediated via slippage
mediated via activation
mediated via phosphorylation
mediated via downregulation
mediated via integrin
regulated via binding
facilitated via binding
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