ArticleInternational journal of molecular sciences2017
Potential Roles of Intrinsic Disorder in Maternal-Effect Proteins Involved in the Maintenance of DNA Methylation.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- PGC7 maintains the pluripotency of F9 embryonic carcinoma cells by promoting Nanog translation.Acta biochimica et biophysica Sinica · 2025Article
- PGC7 regulates maternal mRNA translation via AKT1-YBX1 interactions in mouse oocytes.Cell communication and signaling : CCS · 2024Article
- Methylation is maintained specifically at imprinting control regions but not other DMRs associated with imprinted genes in mice bearing a mutation in theFrontiers in cell and developmental biology · 2023Article
- The zinc-finger transcription factor LSL-1 is a major regulator of the germline transcriptional program in Caenorhabditis elegans.Genetics · 2022Article
- Hemimethylation of CpG dyads is characteristic of secondary DMRs associated with imprinted loci and correlates with 5-hydroxymethylcytosine at paternally methylated sequences.Epigenetics & chromatin · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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Abstract
DNA methylation is an important epigenetic modification that needs to be carefully controlled as a prerequisite for normal early embryogenesis. Compelling evidence now suggests that four maternal-effect proteins, primordial germ cell 7 (PGC7), zinc finger protein 57 (ZFP57), tripartite motif-containing 28 (TRIM28) and DNA methyltransferase (cytosine-5) 1 (DNMT1) are involved in the maintenance of DNA methylation. However, it is still not fully understood how these maternal-effect proteins maintain the DNA methylation imprint. We noticed that a feature common to these proteins is the presence of significant levels of intrinsic disorder so in this study we started from an intrinsic disorder perspective to try to understand these maternal-effect proteins. To do this, we firstly analysed the intrinsic disorder predispositions of PGC7, ZFP57, TRIM28 and DNMT1 by using a set of currently available computational tools and secondly conducted an intensive literature search to collect information on their interacting partners and structural characterization. Finally, we discuss the potential effect of intrinsic disorder on the function of these proteins in maintaining DNA methylation.
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