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It is mediated by sequential activation of an E1-activating enzyme (the SAE1/SAE2 heterodimer), an E2-conjugating enzyme (UBC9), and several E3 protein ligases that confer substrate specificity.
The classic extrinsic (CD95/Fas receptor) apoptotic pathway is activated by soluble Fas ligand (Fas-L) binding to the CD95 or Fas receptor that in turn activates caspase-8 followed by sequential activation of executioner caspases-7 and -3 resulting in cell death (type I cells) [ 9, 10].
We previously demonstrated that activity-dependent dendritic growth in hippocampal neurons is mediated by sequential activation of NMDA receptors, CaMKK, CaMKI, Ras, MEK/ERK, and CREB-dependent transcription of Wnt2 (Wayman et al. 2006).
Similarly, ES cell differentiation pathways are typically directed, in part, by sequential activation of receptor-mediated intracellular signaling pathways by peptides and other molecules [6], [7], [8].
Recent evidences suggest that ras signaling can upregulate cyclin D1 and Cdk 4 assembly by sequential activation of ras, raf-1, ERK pathway [36].
MAPK and PI3K signaling are involved in activation of several membrane signaling molecules followed by sequential activation of protein kinases which involves highly regulated and modulated cascades of phosphorylation events [56].
Similar(46)
Those events were then followed by sequential activations of signal transduction pathways leading to cell death and multiple organ dysfunction and failure.
The cell cycle progression depends on a cascade of enzymes by sequential activation and inactivation of cyclin, cyclin-dependent kinases (CDKs), and cyclin-dependent kinase inhibitors (CDKIs) [ 18].
In all likelihood, homeobox genes control mammary gland development and function by sequential activation or inactivation of specific sets of homeobox genes at specific developmental transition points.
The mammalian cell cycle is regulated by sequential activation and inactivation of a highly conserved family of cyclin dependent kinases (CDKs); progression through early to mid-G1 is dependent on CDK4 and possibly CDK6, while progression through late G1 and the S phase requires activation of CDK2.
They are classically activated following ligand receptor interaction by the sequential activation of a linear cascade of protein kinases, including Ras, Raf-1, MEK, and the MAPKs ERK-1 and ERK-2 (Puri and Siegel, 1993; Smerz-Bertling and Duschl, 1995) on the one hand and PI 3-kinase and Akt on the other hand (Franke et al, 1997; Fahy et al, 2003).
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by sequential removal of
by sequential adsorption of
by sequential application of
by sequential treatment of
by sequential anionicpolymerization of
by sequential smoothing of
by sequential addition of
by sequential impregnation of
by sequential compartmentalisation of
by sequential implantation of
by sequential exposure of
by sequential transduction of
by sequential injection of
by sequential sputtering of
by sequential release of
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