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PstPcD38G and PstPcD229G were efficiently phosphorylated by both PknAc and PknBc (Figure 3A), whereas faint signal on PstPcR20G was observed owing to its partial phosphatase activity.
Moreover, the analysis of early markers for immature progenitors showed that at 1% O2 nestin expression was only slightly down-regulated with differentiation and that a significant fraction of cells co-expressed nestin and GFAP whereas faint levels of nestin were detectable at other oxygen concentrations.
The H3K4me3 was nearly lost from the nptII coding region, whereas faint H3K9me2 signals appeared (Fig. 5B).
The results showed that Plexin-B1 expression levels were the highest in the SKOV3, whereas faint Plexin-B1 expression was found in the OV2008 cells.
Ferrochelatase was predominantly immunolocalised in the majority of neurons and astrocytes in normal brain specimens, whereas faint staining was detected in neoplastic astrocytes in glioblastoma specimens.
Surprisingly, bright RAD51 foci induced by MMC were abolished in cells overexpressing both RAD51 and BRC4, whereas faint foci could still be observed (Fig. 8D and E).
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As shown in Fig. 3, dark colored colonies were observed on the membrane filter of K. aerogenes which was placed on the filter papers soaked in probe solution, whereas only faint colonies were visible on the membrane filter of K. aerogenes without probe 1.
In untreated fronto-cortical neurons, punctate Homer1b staining was clearly evident along the dendrites whereas only faint staining was detectable in dendritic shafts; the majority of Homer1b clusters (83.3±6.5%) were juxtaposed to synaptophysin-positive puncta, indicating synaptic localization of Homer1b in mature neurons.
In contrast, BrFLC2 expression in P11 was strong, whereas very faint in C634.
Importantly, STEAP4 mRNA was highly expressed in all four RA synovia whereas only faint bands were noted for other STEAP families.
Pt 02 did not show full‐length dystrophin in pre‐treatment sample, whereas a faint band corresponding to full‐length dystrophin was observed with anti‐mandys18 and manex46e antibodies only in post‐treatment samples (Fig 3F).
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