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α-Tocopherol treatments showed significant increases in both PPARγ (1.4- to 2.2-fold, P <.01) and NF-κB p50 (1.3- to 1.5-fold, P <.005) DNA binding activities compared with vehicle control.
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Interestingly, mutant T397A showed increased binding activity compared with that of the wild type (Fig. 8K), probably resulting from the removal of certain structure constraints by replacing the bigger "wall" (T397) with a smaller one (alanine) (see Discussion).
The observed differences in binding activity compared with Korhonen et al. could be explained as described above for hexamerization.
In contrast, in mice treated with clonidine we found no difference in NF-κB binding activity compared with mice receiving placebo injections with saline (Data not shown).
It was clearly shown that HIV-1 Tat protein significantly induced NF-κB DNA binding activity compared with control in a time-dependent fashion.
Type 2 diabetes showed increased NF-κB p65-dependent DNA binding activity compared with control subjects (P < 0.01) (Fig. 2 I).
The results showed that PDTC and PD98059 pretreatment noticeably decreased HIV-1 Tat-induced NF-κB DNA binding activity compared with HIV-1 Tat protein treatment alone.
In C2C12 myotubes for PPAR γ knockdown, neither 400 µM EPA nor DHA affected the levels of p-I κ B α, total I κ B α or NF κ B DNA binding activity compared with BSA (P > 0.05).
In C2C12 myotubes transfected with PPAR γ Stealth RNAi oligonucleotide, treatment with 400 μM EPA or 400 μM DHA for 24 h did not affect the levels of p-I κB α or total I κB α), NF κB DNA binding activity), compared with BSA (P > 0.05).
More importantly, treatment of AC16 cells with TNF-α inhibited AP-1 DNA-binding activity compared with control cells.
The Halaban group reported that high E2F1 level in melanoma cells was associated with a fivefold higher DNA-binding activity compared with melanocytes in culture.
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