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In addition, expression of an activated form of Akt was described to trigger spontaneous adipocyte differentiation of 3T3-L1 preadipose cells [55], [56], in support of a role of Akt in regulating PPARγ in fat cells.
In addition, nutrient deprivation was described to trigger lysosomal proteolysis of I κB α through its binding to heat shock protein 73 (hsc73) and lysosomal glycoprotein 96 (Igp96), a lysosomal membrane receptor.
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Various stress conditions have also been described to trigger the expression of virulence factors [ 21].
Recently, 22 nt miRNAs have been described to trigger siRNA biogenesis from target transcripts in Arabidopsis [ 50, 51].
Triethyl amine (NEt3) has already been described to trigger polymerization of HA at 0 °C (Arslan et al. 2004).
EGFR activation has been described to trigger processes such as proliferation, apoptosis, migration, angiogenesis and differentiation [ 44– 44].
For instance, OGT has been described to trigger the export of TET3 from the nucleus and thus impair its activity [ 71].
Downstream effects of C5a include upregulation of IL-8 [ 7] and other proinflammatory mediators, which have been described to trigger catabolic metabolism of cartilage.
According to this structural feature these proteins are referred to as BH3-only proteins and at least eight members have been described to trigger cell death in mammals (1).
Although Smac mimetic has been described to trigger NF- κB activation, the functional relevance of NF- κB as a pro- or antiapoptotic factor during Smac mimetic-induced apoptosis has been controversially discussed.
In addition to activation of caspases, Smac mimetics have been described to trigger an NF- κB-dependent autocrine/paracrine TNF α loop, which induces cell death by facilitating the formation of a TNF α-induced cytosolic complex II consisting of caspase-8, Fas-associated protein with death domain and RIP1, which drives caspase-8 activation and cell death.
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