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T-cell activation is also associated with prompt induction of long-chain acyl-CoA synthetases and lysophosphatidylcholine acyltransferases, known to catalyze the formation of fatty acyl-CoA.
This expression pattern is similar to that of Gmpgip2 and differs from that of Gmpgip1, Gmpgip3 and Gmpgip4, which all show a more prompt induction following S. sclerotiorum infection [[ 18]].
In addition, the ATM kinase activity mediates the prompt induction of various signaling pathways with some of these events leading to either cellular apoptosis or cell cycle arrest [ 4].
The comparison of the three GEPs accepted revealed prompt induction of numerous genes after 17 min ex vivo, which included upregulation of 363 genes >2-folds, 34 genes >3-folds, 10 genes >4-folds, 7 genes >5-folds and 3 genes >10-folds compared with the reference sample frozen immediately following aspiration.
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Likewise, increased DPP signaling caused by a constitutively active Tkv receptor (F ) or ectopic DPP ligand expression (G ) also prompts induction of the p53 reporter.
Recent evidence suggests that high-mobility group box 1 (HMGB1) prompted induction of proinflammatory mediators, including TNF- α, IL-1 β, and cyclooxygenase-2 (COX-2), and contributed to postischemic brain damage [ 39– 41].
On the other hand, binding of RANKL to RANK prompts induction of several intracellular pathways by this receptor, leading to activation of key transcription factors, most notably NF-κB.
Prompt fluorescence induction curves also demonstrated the suppression of fluorescence decay after reaching the maximum due to ΔpH dependent nonphotochemical quenching (qE = (F M – F 6s )/F V )).
Multiple physiological systems, therefore, operate to detect fluctuations in glucose levels and to prompt the induction of apposite counter-regulatory responses, including ingestive behaviour.
It was observed that CO441 response was characterized not only by a constitutive expression, but also by a prompt and enhanced induction of some key genes associated with resistance mechanisms, antioxidant process, hormone signaling, signal transduction cascades and secondary metabolism.
The observation that ser-15 phosphorylation is required for p21 induction prompted us to investigate its role in G1 arrest [26], [28].
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