Exact(1)
On the contrary, the expression of Opn4x and Opn4m was differentially affected by these hormones: α-MSH increased melanopsin expression while melatonin effects depended on the time when it was applied, dramatically abolishing their temporal oscillations and decreasing their expression levels during the light phase.
Similar(59)
Of interest, substitution of Q396N maintained the binding affinity to CXCR4, whereas, replacement of N398Q dramatically abolished CXCR4 binding.
PBIT, the selective NO synthetase inhibitor, could dramatically abolished the inhibiting effects of microglia and MLCs (Figure 5b).
We found that the HIF1α accumulation could be dramatically abolished by ascorbate treatment in comparison to the control untreated OKF6 cells (Figure 4D).
Deletion of E2F C/D (pGL3-ABSp1, pGL3-AB), E2F A/C/D (pGL3-B) or E2F D (pGL3-ABC) dramatically abolished the E2F1-induced promoter activity, suggesting the E2F D site or surrounding sequences could play a critical role in E2F1-mediated CDT2 expression (Fig. 4B).
Their substitution by a charged arginine residue dramatically abolished chloride currents.
In contrast, PI3K/Akt inhibitor LY294002 dramatically abolishes Mcl-1 levels and induces c-PARP1.
As revealed in Figures 7f and g, overexpression of JunB can augment this IRE1a inhibition, whereas knocking down JunB using the siRNA approach dramatically abolishes this IRE1a inhibition.
Deletion of three amino acids in a consensus linker (TGEKP > TG) between finger-7 and the 6 × Histidine-tag in the C-terminal also dramatically abolished their binding affinity.
However, in three LCLs with both SDHD variants (either G12S or H50R) and PTEN mutations (insertion, truncation or early translation termination), which dramatically abolished PTEN function, no significant induction of apoptosis was observed (Fig. 6C).
The pretreatment with α-bungarotoxin or tubocurarine chloride dramatically abolished nicotine-increased hu-imDCs mediated PBMC proliferation, which revealed about 26.65% and 43.26% inhibitory rates, respectively,), indicating that nicotine exposure-increased hu-imDCs-mediated PBMC proliferation is α7 nAchR-dependent.
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