| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T99 |
0-81 |
Sentence |
denotes |
Histone methylation does not appear to exhaust the epigenetic regulation of ACE2. |
| T100 |
82-230 |
Sentence |
denotes |
Notably, the NAD+-dependent deacetylase SIRT1 binds to ACE2 promoter favoring its transcription during cellular energy stress (Clarke et al., 2014). |
| T101 |
231-311 |
Sentence |
denotes |
Two recent unrefereed preprints highlighted other epigenetic mechanisms at play. |
| T102 |
312-516 |
Sentence |
denotes |
Corley et al.1 pointed out that DNA methylation across three CpG islands in the ACE2 promoter was lower in lung epithelial cells compared to other cell types, suggesting high transcription in lung tissue. |
| T103 |
517-719 |
Sentence |
denotes |
These findings are in excellent agreement with the reported inverse correlation between ACE2 transcription and promoter methylation in tumors, which will be discussed in section ACE2 and Other Diseases. |
| T104 |
720-902 |
Sentence |
denotes |
This correlation is also supported by the observation that in children ACE2 is normally hypermethylated and poorly expressed either in the lung and in other organs (Pruimboom, 2020). |
| T105 |
903-1124 |
Sentence |
denotes |
Glinsky (2020) addressed the epigenetic role of Vitamin D on ACE2 expression, showing by gene set enrichment analysis that the Vitamin D receptor (VDR) should be involved in a set of regulatory pathways conveying on ACE2. |
| T106 |
1125-1334 |
Sentence |
denotes |
More specifically, VDR activation would downregulate ACE2, thus affording a potential reason for the alleged beneficial role of Vitamin D in COVID-19 (section ACE2 and the Inflammatory Response to Sars-CoV-2). |
