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By contrast, a very strong enrichment of the methylated marks was detected on tGgIdas in larval tissues (Fig. 3A C).
Co-variation between marks was detected and the data suggested that H3K4me3 differences could help re-establish H3K14ac differences after reprogramming.
A comparably low amount of PC and PH marks was detected on tGgIdas and tGgDId in the follicle cells (Fig. 4B′ and C′).
Interestingly, no ANRASSF1 effect on histone marks was detected either on the promoter of the RASSF1C isoform or on the promoters of four other genes in the tumour suppressor gene cluster at the 3p21.3 locus [ 70].
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Also, no weld lines, meld lines or sink marks were detected with new design of the edge gate.
As expected for ES cells, all silencing histone methylation marks were detected at rather low levels throughout the rDNA locus [31].
Decreases in permissive H3K4m3 and H3Km2 marks were detected only in the lung.
Consistent with our hypothesis, significant reductions in H3K27me3 chromatin marks were detected in association with ABI3 and LEC1 genomic sequences only in chromatin from hsi2-2 LUC but not hsi2-4 LUC mutant seedlings and genes such as LEC2 and L1L, which are not misregulated in either hsi2 mutant allele alone, also showed no change in H3K27me3 marks in these mutant backgrounds.
Open chromatin marks were detected to be significantly enriched at their promoters (Fisher's exact test, H3K4me3, p-value < 2.2e-16; H3K4me2, p-value < 2.2e-16) and gene bodies (Wilcoxon test, H3K36me3, p-value<2.2e-16; H3K79me2, p-value< 2.2e-16), confirming active transcription of these genomic regions in human ES cells [ 20, 21] (Additional File 3).
In fact, loss of this mark was detected in early passage cultures before any nuclear defects were observed suggesting heterochromatin defects precede nuclear defects [ 27].
After incubation, the medium was removed and cells were lysed, histones were extracted and histone carrying the acetylation mark was detected following the manufacturer's instructions (PerkinElmer; Cat number AL714 A/C kit assay).
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