ReviewGenes & diseases2025
TET1: The epigenetic architect of clinical disease progression.
Review in Genes & diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed.
- TET Enzymes as Epigenetic Integrators in Intestinal Immunity, Inflammation, and Disease.Journal of personalized medicine · 2026Review
- Enhanced anti Pseudomonas aeruginosa efficacy of niosomal-encapsulated Frondoside A from sea cucumber: a novel biotechnological approach.BMC biotechnology · 2026Article
- KAT6A regulates osteoclast differentiation and bone resorption through TET1-mediated TRPV4 expression.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- TET1 suppresses hepatocellular carcinoma progression by modulating the PI3K/Akt signaling pathways.Scientific reports · 2026Article
- Hypermethylation of lysosomal-associated genes LAMP1 and LAMP2 compromises lysosome function in patients with acute lymphoblastic leukemia.Immunologic research · 2025Article
- TET1 modulates trophoblast function by regulation of ODC1 in preeclampsia.Scientific reports · 2025Article
- Molecular Mechanisms and Therapeutic Perspectives of Gut Microbiota, Autophagy, and Apoptosis in Cholangiocarcinoma Pathophysiology.International journal of molecular sciences · 2025Review
- Polarization of Tumor Cells and Tumor-Associated Macrophages: Molecular Mechanisms and Therapeutic Targets.MedComm · 2025Review
- The transcriptional regulators GATA6 and TET1 regulate the TGF-β pathway in cancer-associated fibroblasts to promote breast cancer progression.Cell death discovery · 2025Article
- TET1-mediated DNA demethylation suppresses migration of goat placental trophoblast cells.Journal of animal science · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ten-eleven translocation 1 (TET1) protein, a member of the human α-ketoglutarate-dependent dioxygenase TET family, functions as a 5-methylcytosine hydroxylase with a strong affinity for genomic regions enriched with 5'-CpG-3' dinucleotides, particularly CpG islands. TET1 is critical in initiating DNA demethylation and maintaining a balanced interaction between demethylation and DNA methylation, which is essential for genomic methylation stability and precise epigenetic regulation. By removing methyl groups from specific tumor suppressor genes, TET1 can influence their expression. This review summarizes the latest advancements in TET1 research, emphasizing its role in demethylation mechanisms and its significance in regulatory processes related to clinical conditions. TET1 is a crucial mediator of demethylation, although the precise details of this mechanism are not yet fully understood. Additionally, TET1 plays a key role in inhibiting tumor progression, but its effects vary across different tumors. This variability arises from its interactions with diverse signaling pathways, where it can function either as an antagonist or a promoter. The role of TET1 remains controversial in certain cancer types, and its potential oncogenic functions have attracted growing interest, opening new avenues for investigation.
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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 Socratic graph.