ArticleNature communications2019
SMARCAD1 ATPase activity is required to silence endogenous retroviruses in embryonic stem cells.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 2,390 citations in OpenAlex.
- Loss of SMARCAD1 Mitigates Tauopathy.Aging cell · 2026Article
- SFPQ directs histone H3.3 deposition to R-loops in DNA repeats to protect genome stability.Nature communications · 2026Article
- Requirements for establishment and epigenetic stability of mammalian heterochromatin.Molecular cell · 2025Article
- Article
- The HP1 box of KAP1 organizes HP1α for silencing of endogenous retroviral elements in embryonic stem cells.Nature communications · 2025Article
- Article
- Interferon response and epigenetic modulation byScience advances · 2024Article
- ChAHP2 and ChAHP control diverse retrotransposons by complementary activities.Genes & development · 2024Article
- SETDB1 as a cancer target: challenges and perspectives in drug design.RSC medicinal chemistry · 2024Review
- Wybutosine hypomodification of tRNAphe activates HERVK and impairs neuronal differentiation.iScience · 2024Article
- Context-specific functions of chromatin remodellers in development and disease.Nature reviews. Genetics · 2024Review
- Article
- HIRA vs. DAXX: the two axes shaping the histone H3.3 landscape.Experimental & molecular medicine · 2024Review
- Regulation of endogenous retroviruses in murine embryonic stem cells and early embryos.Journal of molecular cell biology · 2024Review
- Article
- H3K4 trimethylation regulates cancer immunity: a promising therapeutic target in combination with immunotherapy.Journal for immunotherapy of cancer · 2023Review
- Comprehensive Analysis and Drug Modulation of Human Endogenous Retrovirus in Hepatocellular Carcinomas.Cancers · 2023Article
- Histone exchange sensors reveal variant specific dynamics in mouse embryonic stem cells.Nature communications · 2023Article
- Differential effect of histone H3.3 depletion on retroviral repression in embryonic stem cells.Clinical epigenetics · 2023Article
- Trim28 citrullination maintains mouse embryonic stem cell pluripotency via regulating Nanog and Klf4 transcription.Science China. Life sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endogenous retroviruses (ERVs) can confer benefits to their host but present a threat to genome integrity if not regulated correctly. Here we identify the SWI/SNF-like remodeler SMARCAD1 as a key factor in the control of ERVs in embryonic stem cells. SMARCAD1 is enriched at ERV subfamilies class I and II, particularly at active intracisternal A-type particles (IAPs), where it preserves repressive histone methylation marks. Depletion of SMARCAD1 results in de-repression of IAPs and adjacent genes. Recruitment of SMARCAD1 to ERVs is dependent on KAP1, a central component of the silencing machinery. SMARCAD1 and KAP1 occupancy at ERVs is co-dependent and requires the ATPase function of SMARCAD1. Our findings uncover a role for the enzymatic activity of SMARCAD1 in cooperating with KAP1 to silence ERVs. This reveals ATP-dependent chromatin remodeling as an integral step in retrotransposon regulation in stem cells and advances our understanding of the mechanisms driving heterochromatin establishment.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.