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This study was designed in order to determine whether these beneficial flow patterns are replicated in vivo in PCG.
Likewise, in PCG signals, murmurs appear overlapped with the cardiac beat, and sometimes cannot be easily distinguished even by the human ear [3].
These findings suggest that the abnormalities in the development of the trabecular meshwork in PCG may result from diminished or absent metabolism of important endogenous substrates in the ciliary epithelium due to non-functional CYP1B1 enzyme.
Similarly, the accumulation of ROS triggers a reduction in PcG protein levels downstream of activated JNK signaling [50], [51].
Similar studies have asked whether mutations in PcG proteins are dominant or dosage sensitive suppressors of TPE[38], [44], [45].
Cell fate transformation is a hallmark of mutation in PcG and TrxG genes, and is how the genes in these groups were originally identified.
Mutations in PcG and trxG genes disrupt the specification of anterior-posterior (A/P) positional information and lead to homeotic transformations.
We assumed that activation of differentiation in NT2 cells would require substantial epigenetic modulation, especially changes in PcG presence, histone modification patterns and also DNA methylation.
Consistent with the hypothesized role of ETP proteins in PcG and trxG recruitment to target chromatin, Asx is a nuclear protein that binds distinct loci on polytene chromosomes [30].
We will keep here the term ETP for those maintenance proteins that play a dual role in PcG and TrxG functions without belonging to any PcG or TrxG complexes identified so far.
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A compromise in PcG-associated HMTase activity was also observed in Asxl2−/− hearts, which exhibit reduced global level of H3K27me3 (Fig. 5F).
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