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). |