ArticleWorm2014
Maintenance of cell fates through acetylated histone and the histone variant H2A.z in C. elegans.
Article in Worm, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed, 3 citations in OpenAlex.
- Maintenance of cell fates and regulation of the histone variant H3.3 by TLK kinase inBiology open · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maintenance of cell fates is essential for the development and homeostasis of multicellular organisms and involves the preservation of the expression status of selector genes that control many target genes. Epigenetic marks have pivotal roles in the maintenance of gene expression status, as occurs with methylation on lysine 27 of histone H3 (H3K27me) for Hox gene regulation. In contrast, because the levels of histone acetylation decrease during the mitotic phase, acetylated histone has not been believed to contribute to the maintenance of cell fates. Because members of the bromodomain and extra terminal (BET) family bind to acetylated histones localized on mitotic chromosomes, it is possible that they may regulate the transcriptional status of genes throughout the cell cycle. In this commentary, we discuss the recent analyses of C. elegans BET family protein BET-1, which contributes to the maintenance of cell fates through the histone H2A variant HTZ-1/H2A.z. This mechanism represses transcription of selector genes in the genomic region where lysine 27 of histone H3 (H3K27) is demethylated by histone demethylase UTX-1. We discuss the possibility that BET-1 and HTZ-1 maintain the poised state of RNA polymerase II in the cell such that it is ready to respond to differentiation signals.
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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.