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Insufficient degradation due to altered protein structure or proteasome inhibition may trigger cell death.
Furthermore, we hypothesize that, like in the solid tumors mentioned above, AQP5 may trigger cell proliferation in leukemic cells.
Further, the stimulation of G protein-coupled P2Y receptors may trigger cell death by promoting the release of glutamate from nerve terminals and/or astrocytes [22] shown in vivo or by the activation of early apoptotic enzymes e.g., active caspase 3 via P2Y1 receptors [23].
These described changes may trigger cell damage and death.
It is conceivable that the p21/cyclin D interval variations may trigger cell cycle progression.
The accumulation of chlorophyll breakdown products may trigger cell death [ 122].
Similar(38)
Upon ligand binding, integrins may trigger cells to secrete growth factors and/or cytokines, which in turn can bind to their receptors in an autocrine or paracrine manner to induce further signaling.
The downstream displacement of the nucleus directly contributes to the establishment of planar cell polarity in endothelium (Fig. 4d) and may also trigger cell signaling events eventually leading to relocation of MTOC by cytoskeletal motors (McCue et al., 2006; Morgan et al., 2011; Tzima et al., 2003).
FUS tumour ablation creates a large amount of tumour antigens in the form of necrotic cells and damaged tumour cells, which may trigger dendritic cell activation.
In the presence of natural killer cells they may trigger endothelial cell apoptosis [ 31] or lead to the induction of effector mechanisms via antibody-dependent cellular cytotoxicity and complement activation [ 32, 33].
The hypoxic state that we have now identified in db/db islets and the induction of ER stress and apoptosis that we observed in Min6 cells following exposure to 1% O2 suggest that hypoxia may trigger β-cell dysfunction and cell loss during the progression of type 2 diabetes.
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