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Amplified RNAs for the three control clones treated with Dex were then mixed in equal proportions to obtain a "Control-treated pool".
The proliferative response to C1R.d/αGC was significantly inhibited in the responding NKT clones treated with anti-CD1d in a dose-dependent manner (Figure 6B C).
Reactivating K3− clones, treated with phosphonoacetic acid to prevent any post-induction spread of lytic infection, showed significantly better epitope presentation than K3+ (Fig. 6c).
Similarly, increased cAMP levels in Th2 and Th0 clones treated with prostaglandin E2 (PGE2) had no effect on IL-4 production while IL-5 synthesis was inhibited.
Immunoprecipitation experiments of HIF-1α protein were also perfomed in two other melanoma cell lines, JR8 and PLF2, and their bcl-2 derivative stably clones treated with MG132 obtaining similar results ( Figure 3C,D ) and thus generalizing the ability of bcl-2 protein to interact with HIF-1α protein.
However, the clones treated with shRNA against elastase had reduced elastase expression.
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Each concentration of TNF- α resulted in the same level of LTR-driven GFP expression (data not shown); therefore, each panel within Figure 1(a) represents a separate cell clone treated with TNF- α (20 ng/mL).
Each concentration of IL-1 β resulted in similar levels of LTR-driven GFP expression (data not shown); therefore, each panel within Figure 2(a) represents a separate cell clone treated with IL-1 β (20 ng/mL).
For drug response, no marked differences were found in the dose response curves of RIF-1 clones treated in vitro with adriamycin.
Parental cells, two vector control clones, and three T βRII clones were treated with TGF- β for 90 min and cell lysates were subjected to Western blot analyses by antiphospho-Smad2 antiphospho-Smad3mantibodiesdies.
For each clone, kinetic treatment experiments were performed; clones were treated with 500 nmol/l TSA or 500 µmol/l 5-AzaC at five time points (0, 8, 24, 32, and 48 hours).
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