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DNA methylation, post-translational modification of histones and chromatin remodeling are nuclear mechanisms implicated in epigenetic control of gene expression.
All factors relevant to tissue differentiation, including cell adhesion and shape, extracellular stimuli and transcriptional control, modulate gene expression and, thus, some of them are likely to impact on nuclear mechanisms of epigenetic control.
Post-translational modification of histones, ATP-dependent chromatin remodeling, and DNA methylation are interconnected nuclear mechanisms that ultimately lead to the changes in chromatin structure necessary to carry out epigenetic gene expression control.
Elements critical for tissue differentiation, like extracellular stimuli, adhesion and cell shape properties, and transcription factors all contribute to the modulation of gene expression and thus, are likely to impinge on the nuclear mechanisms of epigenetic gene expression control.
Focusing on yeast as a model system, we will review here how nuclear mechanisms ensure the proper assembly and maturation of mRNPs for their release in the cytoplasm, and highlight how these mechanisms are exploited to shape the RNA polymerase II transcriptome.
Cerebellar cortical and nuclear mechanisms in learning were recently dissociated by analyzing memory consolidation.
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This paper presents an approximation approach to predict the core characteristics based on parametric survey and an analysis of nuclear mechanism in a conceptual nuclear design for enhanced transuranics (TRU) burning mixed oxide fueled and sodium cooled fast reactor which can be realized in the near future.
We have suggested that the relative dependence of cerebellum-dependent forms of learning on cortical and nuclear mechanism may relate to the frequency component content of the learned responses.
Rac3 can also activate NFκB through a nuclear mechanism, serving as a nuclear coactivator for NFκB-dependent transcription.
Hence, it is possible that there is a nuclear mechanism for Aβ-mediated RPE cell death and dysfunction.
Chromatin remodeling subsequent to DNA double-strand breaks (Suberbielle et al., 2013) is another potential nuclear mechanism for LTM storage.
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