ArticlePloS one2020
Mouse dead end1 acts with Nanos2 and Nanos3 to regulate testicular teratoma incidence.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Dead-End protein expression, function, and mutation in cancer: a systematic review.Molecular biology reports · 2025Pooled it
- DND1-NANOS3 shapes the PGC transcriptome via a heptanucleotide sequence in mRNA 3' UTRs.Molecular cell · 2026Article
- Primordial Germ Cell Development in Teleosts: Their Origin, Fate and Role in Sex Determination.Stem cell reviews and reports · 2026Review
- A Nanos3-containing protein complex can activate RNA translation in primordial germ cells in vivo.EMBO reports · 2026Article
- Driving precision medicine in testicular germ cell tumors: from preclinical models to clinical applications.Therapeutic advances in medical oncology · 2026Review
- The DND1-NANOS3 complex shapes the primordial germ cell transcriptome via a heptanucleotide sequence in mRNA 3' UTRs.bioRxiv : the preprint server for biology · 2025Article
- Article
- Loss of Dead end1 induces testicular teratomas from primordial germ cells that failed to undergo sexual differentiation in embryonic testes.Scientific reports · 2023Article
- Emerging Roles of NANOS RNA-Binding Proteins in Cancer.International journal of molecular sciences · 2022Article
- The Role of DND1 in Cancers.Cancers · 2021Review
- Testicular germ cell tumors arise in the absence of sex-specific differentiation.Development (Cambridge, England) · 2021Article
- The involvement of bioactive factors in the self-renewal and stemness maintenance of spermatogonial stem cells.Molecular and cellular biochemistry · 2021Review
- MC4R mutant mice develop ovarian teratomas.Scientific reports · 2021Article
- High DND1 Level Indicates a Poor Prognostic Factor in Prostate Cancer.Disease markers · 2021Article
- Heading towards a dead end: The role of DND1 in germ line differentiation of human iPSCs.PloS one · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spontaneous testicular teratomas (STTs) derived from primordial germ cells (PGCs) in the mouse embryonic testes predominantly develop in the 129 family inbred strain. Ter (spontaneous mutation) is a single nucleotide polymorphism that generates a premature stop codon of Dead end1 (Dnd1) and increases the incidence of STTs in the 129 genetic background. We previously found that DND1 interacts with NANOS2 or NANOS3 and that these complexes play a vital role in male embryonic germ cells and adult spermatogonia. However, the following are unclear: (a) whether DND1 works with NANOS2 or NANOS3 to regulate teratoma incidence, and (b) whether Ter simply causes Dnd1 loss or produces a short mutant DND1 protein. In the current study, we newly established a conventional Dnd1-knockout mouse line and found that these mice showed phenotypes similar to those of Ter mutant mice in spermatogenesis, oogenesis, and teratoma incidence, with a slight difference in spermiogenesis. In addition, we found that the amount of DND1 in Dnd1+/Ter embryos decreased to half of that in wild-type embryos, while the expression of the short mutant DND1 was not detected. We also found that double mutants for Dnd1 and Nanos2 or Nanos3 showed synergistic increase in the incidence of STTs. These data support the idea that Ter causes Dnd1 loss, leading to an increase in STT incidence, and that DND1 acts with NANOS2 and NANOS3 to regulate the development of teratoma from PGCs in the 129 genetic background. Thus, our results clarify the role of Dnd1 in the development of STTs and provide a novel insight into its pathogenic mechanism.
Indexed as
Identifiers
What Socratic 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 Socratic graph.