SETDB1 bound to TRIM28 trimethylates lysine-9 of histone H3 ...
| created | [InstanceEdit:9843639] May, Bruce, 2023-09-08 |
| dbId | 9843618 |
| displayName | SETDB1 bound to TRIM28 trimethylates lysine-9 of histone H3 ... |
| literatureReference |
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| modified | [InstanceEdit:9910913] May, Bruce, 2024-05-23 |
| schemaClass | Summation |
| text | SETDB1 bound to TRIM28 trimethylates lysine-9 of histone H3 (H3K9) (Schultz et al. 2002, Wang et al. 2003, Basavapathruni et al. 2016). ATF7IP (hAM, mAM) binds SETDB1 in the nucleus and enhances the methyltransferase activity of SETDB1 (Wang et al. 2003, Basavapathruni et al. 2016, also inferred from mouse homologs in Tsusaka et al. 2019, 2020). In mouse embryos, knockout of Trim28 causes a reduction in H3K9 trimethylation and increased expression of transposable elements such as intracisternal A-type particels (IAPs) (Rowe et al. 2010). In mouse embryonic stem cells, SETDB1 (Matsui et al. 2010) and the SETDB1-interacting region of ATF7IP Tsusaka et al. 2020) are required for silencing of retrotransposons. In mouse embryonic stem cells, endogenous retroviruses are targeted by KRAB?ZFPs, TRIM28, and SETDB1 and become DNA methylated, likely due to interaction between TRIM28 and DNA methylases (Rowe et al. 2010, Rowe et al. 2013). DNA methylation and H3K9 trimethylation regulate distinct sets of loci in mouse embryonic stem cells (Karimi et al. 2011). Heterochromatin initiated by a KRAB-ZFP can spread across several tens of kilobases (Groner et al. 2010). |
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