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These genes are stably repressed in stem cells and non-neural tissues following binding of the REST complex that consists of several proteins including REST, JARID1C and other chromatin modifying enzymes [7].
Elucidation of the REST complex, and comparison of chromatin marks and gene expression levels in control and REST-deficient stem cells, shows that REST target genes are poised by a mechanism independent of Polycomb, even at promoters which bear the H3K27me3 mark.
DOI: http://dx.doi.org/10.7554/eLife.04235.012 The presence of HDACs in the REST complex predicted increased H3K9ac enrichment at RE1 sites in Rest −/− ESCs, which we observed in 11/16 analyzed genes, with no change in the controls that lacked RE1 sites.
Since Sin3A and coREST bind opposite termini of REST, these overlapping lncRNAs might serve as a scaffold to recruit Sin3A and coREST to the REST complex and/or facilitate the recruitment of other proteins such as histone deacetylases that are common to both corepressors (Ballas and Mandel, 2005; Roopra et al., 2012).
In order to address this issue, an original lumped model of the human torso was developed and coupled to a car seat-head rest complex.
Specifically, we identified Jarid1c, a H3K4me3 demethylase recruited by the REST complex that is essential for neuronal survival and dendritic development [70].
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Binuclear complexes of VO2+, Co2+, Ni2+, Cu2+ and Zn2+ with oxalyl bis(diacetylmonoximehydrazone) were characterized as 2 2 (M L) and an octahedral geometry for VO2+, tetrahedral for Zn2+ and square-planar for the rest complexes were proposed [15].
To test this idea we performed a mass spectrometric analysis of REST complexes using a mouse ESC line that stably expressed both the biotin conjugating enzyme, BirA (Kim et al., 2009), and REST tagged with a biotin acceptor sequence.
To supplement this proteomic approach, and as an independent test for the role of PRC2 members in REST regulation, we used a genome-wide ChIP-seq approach.> -wrap-foot> A Polycomb complex was not represented in our analysis of REST complexes, but it was possible that the streptavidin pull-downs might not co-purify ncRNA-mediated associations.
To better clarify our meaning, we have replaced the sentence in question with the following: "Second, the Polycomb complex member Eed, which is required for H3K27me3 deposition, was absent from the REST complexes characterized by mass spectrometry and co-immunoprecipitation, undermining the likelihood of either repressive complex directly targeting the other".
REST complexes are able to both silence and repress neuronal genes in embryonic neural stem cells through the creation of chromatin environments that contain both repressive and active local epigenetic signatures (Greenway et al. 2007; Sun et al. 2005b; Ballas et al. 2005).
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