PMC:7556165 / 13125-14904 JSONTXT 17 Projects

Annnotations TAB TSV DIC JSON TextAE

Id Subject Object Predicate Lexical cue
T87 0-162 Sentence denotes A recent analysis of public genomic and transcriptomic data outlined the role of histone methylation, a classical epigenetic mark, to regulate ACE2 transcription.
T88 163-324 Sentence denotes Indeed, Li Y. et al. (2020) showed that transcription of ACE2 was significantly upregulated when the histone mutant H3K27M was overexpressed to inhibit H3K27me3.
T89 325-407 Sentence denotes Conversely, overexpression of mutant H3K4/9/36M did not change ACE2 transcription.
T90 408-563 Sentence denotes Trimethylation of K27 on H3 is catalyzed by the polycomb groups (PcG), a group of conserved transcriptional gene repressors (Schuettengruber et al., 2017).
T91 564-626 Sentence denotes PcG proteins assemble into two major complexes: PRC1 and PRC2.
T92 627-751 Sentence denotes The simplest model of PcG activity involves trimethylation of H3 by PRC2 at target gene promoters (Blackledge et al., 2015).
T93 752-1000 Sentence denotes These epigenetic marks recruit PRC1 on DNA, which in turn acts as E3-ligase and ubiquitinates nearby H2A histones (Storti et al., 2019), triggering silencing of gene transcription by local and reversible compaction of chromatin (Illingworth, 2019).
T94 1001-1066 Sentence denotes The catalytic subunit of PRC2 is constituted by the EZH2 protein.
T95 1067-1234 Sentence denotes In agreement with the inverse correlation between ACE2 level and H3K27me3, ACE2 expression in human ESCs was upregulated following EZH2 knock-out (Li Y. et al., 2020).
T96 1235-1298 Sentence denotes On the other side, recovery of EZH2 restored basal ACE2 levels.
T97 1299-1492 Sentence denotes Chromatin immunoprecipitation sequencing (ChIP-seq) showed that EZH2 depletion induced H3K27me3 decrease, with concomitant H3K27ac increase, at ACE2 promoter in human ESCs (Li Y. et al., 2020).
T98 1493-1779 Sentence denotes The role of H3 methylation and acetylation in the epigenetic regulation of ACE2 was also hypothesized by Pinto et al., who demonstrated that co-morbidities such as hypertension, diabetes, and chronic obstructive lung disease increase ACE2 transcription in the lung (Pinto et al., 2020).