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Thomson, J.P. et al. CpG islands influence chromatin structure via the CpG-binding protein Cfp1.
Recent findings suggest that there is abundant TRF2 at telomeres [49] raising the possibility that TRF2 can influence chromatin structure.
c-Myc can also indirectly regulate transcription through up-regulation of histone acetylases, with the potential to globally influence chromatin structure [5].
Our findings cannot be explained simply by GC-content variations in the genome [21] [23], and suggest that long-range periodic VWG signals influence chromatin structure and chromosome function.
These results indicate that these chemicals that influence chromatin structure can enhance the effects of short-term expression of key reprogramming factors in activating expression of the endogenous pluripotency associated transcription factor network.
However, it has been recently described that down-regulation of Myc expression leads to a widespread decrease of active and increase of repressive chromatin marks [60], suggesting that Myc might influence chromatin structure of its target promoters with the same molecular mechanism we describe here for NF-Y.
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Epigenetic mechanisms involving DNA methylation, histone modification, histone variants and nucleosome positioning, and noncoding RNAs regulate cell-, tissue-, and developmental stage-specific gene expression by influencing chromatin structure and modulating interactions between proteins and DNA.
This suggests that Fun30 directly associates with the heterochromatic HMR and the boundary element, influencing chromatin structure there.
It is thought that extensive modification of histone tails determines local chromatin structure, either by influencing chromatin structure directly or by recruitment of modifying factors, such as PcG proteins.
Considering the finding that there is enough TRF2 bound to nuclear chromatin to saturate telomeres [49], it is likely that TRF2 influences chromatin structure at telomeres if it can access nucleosomal chromatin.
Several results indicate that RNA also influences chromatin structure as, first, chromatin-induced gene silencing depends on the RNAi machinery [14] [16] and, second, dosage compensation requires the contribution of specific non-coding RNAs [17], [18].
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