ArticleStem cell reports2022
PIM3-AMPK-HDAC4/5 axis restricts MuERVL-marked 2-cell-like state in embryonic stem cells.
Article in Stem cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- The syntaxin-binding protein STXBP5 regulates progerin expression.Scientific reports · 2024Article
- Species-Specific Transcription Factors Associated with Long Terminal Repeat Promoters of Endogenous Retroviruses: A Comprehensive Review.Biomolecules · 2024Review
- Regulation of endogenous retroviruses in murine embryonic stem cells and early embryos.Journal of molecular cell biology · 2024Review
- The Molecular Impacts of Retrotransposons in Development and Diseases.International journal of molecular sciences · 2023Review
- Dot1l cooperates with Npm1 to repress endogenous retrovirus MERVL in embryonic stem cells.Nucleic acids research · 2023Article
- HDAC4 in cancer: A multitasking platform to drive not only epigenetic modifications.Frontiers in molecular biosciences · 2023Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A minority of embryonic stem cells (ESCs) marked by endogenous retrovirus MuERVL are totipotent 2-cell-like cells. However, the majority of ESCs repress MuERVL. Currently, it is still unclear regarding the signaling pathway(s) repressing the MuERVL-associated 2-cell-like state of ESCs. Here, we identify the PIM3-downstream signaling axis as a key route to repress MuERVL and 2-cell-like state. Downregulation, deletion, or inhibition of PIM3 activated MuERVL, 2-cell genes, and trophectodermal genes in ESCs. By screening PIM3-regulated pathways, we discovered AMPK as its key target. The loss of Pim3 caused an increase in AMPK phosphorylation, which phosphorylated HDAC4/5 and triggered their transfer out of the nucleus in Pim3
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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.