The HUSH complex cooperates with TRIM28 to repress young retrotransposons and new genes
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Summary
A critical role for the HUSH complex is revealed in naïve cells, implicating it in programming epigenetic marks in development and indicating that the Hush complex and TRIM28 co-repress young retrotransposons and new genes rewired by retro transposon noncoding DNA.
- Type
- article
- Published
- 2018-05-04
- Cited by
- 191
- References
- 47
- Access
- Open access
- OpenAlex
- https://openalex.org/W2801545642
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:19231073
Keywords
Retrotransposon, Biology, Genetics, Gene, Chromatin
References
- Histone H3.3 is required for endogenous retroviral element silencing in embryonic stem cells
- Systematic Identification of Factors for Provirus Silencing in Embryonic Stem Cells
- Mice lacking the transcriptional corepressor TIF1beta are defective in early postimplantation development.
- Atrx promotes heterochromatin formation at retrotransposons
- Chromatin at the nuclear periphery and the regulation of genome functions
- PHD domain-mediated E3 ligase activity directs intramolecular sumoylation of an adjacent bromodomain required for gene silencing.
- Embryonic stem cells use ZFP809 to silence retroviral DNAs
- Interplay of TRIM28 and DNA methylation in controlling human endogenous retroelements
- The first mouse mutants of D14Abb1e (Fam208a) show that it is critical for early development
- De novo DNA methylation of endogenous retroviruses is shaped by KRAB-ZFPs/KAP1 and ESET
- Proviral silencing in embryonic stem cells requires the histone methyltransferase ESET
- An evolutionary arms race between KRAB zinc finger genes 91/93 and SVA/L1 retrotransposons
- The ground state of embryonic stem cell self-renewal
- TRIM28 repression of retrotransposon-based enhancers is necessary to preserve transcriptional dynamics in embryonic stem cells
- KAP1 controls endogenous retroviruses in embryonic stem cells
- Loss of Atrx Affects Trophoblast Development and the Pattern of X-Inactivation in Extraembryonic Tissues
- Retrotransposon-Induced Heterochromatin Spreading in the Mouse Revealed by Insertional Polymorphisms
- Methyl‐H3K9‐binding protein MPP8 mediates E‐cadherin gene silencing and promotes tumour cell motility and invasion
- A HUSH for transgene expression
- The Sequence Alignment/Map format and SAMtools
Cited by
- Deregulation of Retroelements as an Emerging Therapeutic Opportunity in Cancer.
- L1 retrotransposition in the soma: a field jumping ahead
- Epigenetic regulation of intragenic transposable elements: a two-edged sword
- KAP1 regulates endogenous retroviruses in adult human cells and contributes to innate immune control
- Antiviral resistance of stem cells
- NP220 mediates silencing of unintegrated retroviral DNA
- How cells hush a viral invader
- Structure of the tripartite motif of KAP1/TRIM28 identifies molecular interfaces required for transcriptional silencing of retrotransposons
- TRIM28 promotes HIV-1 latency by SUMOylating CDK9 and inhibiting P-TEFb
- Dynamic Methylation of an L1 Transduction Family during Reprogramming and Neurodifferentiation
- HUSH, a Link Between Intrinsic Immunity and HIV Latency
- Characterisation of class VI TRIM RING domains: linking RING activity to C-terminal domain identity
- Fam208a orchestrates interaction protein network essential for early embryonic development and cell division.
- Primate immunodeficiency virus Vpx and Vpr counteract transcriptional repression of proviruses by the HUSH complex
- LINE-1 Evasion of Epigenetic Repression in Humans.
- BRCA1 Mediated Homologous Recombination and S Phase DNA Repair Pathways Restrict LINE-1 Retrotransposition in Human Cells
- Structure of KAP1 tripartite motif identifies molecular interfaces required for retroelement silencing
- A cohesin/HUSH- and LINC-dependent pathway controls ribosomal DNA double-strand break repair
- Navigating through the nucleus with a virus.
- HIV-1 Vpr mediates the depletion of the cellular repressor CTIP2 to counteract viral gene silencing
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