ArticleGenes & development2004
Ovca1 regulates cell proliferation, embryonic development, and tumorigenesis.
Article in Genes & development, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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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.
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Who cites it
61 citing papers in PubMed, 106 citations in OpenAlex.
- A pediatric case of diphthamide biosynthesis 1 gene defect presenting with developmental delay, short stature, dysmorphic features, and sparse hair (Loucks-Innes syndrome): a case report.Journal of medical case reports · 2025Article
- DNAJC24 suppresses breast cancer malignancy and serves as a prognostic biomarker.Cancer cell international · 2025Article
- Loss of Diphthamide Increases DNA Replication Stress in Mammalian Cells by Modulating the Translation of RRM1.ACS central science · 2024Article
- Diphthamide deficiency promotes association of eEF2 with p53 to induce p21 expression and neural crest defects.Nature communications · 2024Article
- DPH1 and DPH2 variants that confer susceptibility to diphthamide deficiency syndrome in human cells and yeast models.Disease models & mechanisms · 2023Article
- eEF2 diphthamide modification restrains spurious frameshifting to maintain translational fidelity.Nucleic acids research · 2023Article
- Oxygen toxicity causes cyclic damage by destabilizing specific Fe-S cluster-containing protein complexes.Molecular cell · 2023Article
- Translational fidelity and growth of Arabidopsis require stress-sensitive diphthamide biosynthesis.Nature communications · 2022Article
- Sequential development of embryoblast-like memory entities in human cancer tissues: an evolutionary self-repair structure with pluripotentiality.American journal of translational research · 2022Article
- Diphthamide promotes TOR signaling by increasing the translation of proteins in the TORC1 pathway.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Iron in Translation: From the Beginning to the End.Microorganisms · 2021Review
- Diphthamide-deficiency syndrome: a novel human developmental disorder and ribosomopathy.European journal of human genetics : EJHG · 2020Article
- Identification of the transcription factor Miz1 as an essential regulator of diphthamide biosynthesis using a CRISPR-mediated genome-wide screen.PLoS genetics · 2020Article
- DPH1 syndrome: two novel variants and structural and functional analyses of seven missense variants identified in syndromic patients.European journal of human genetics : EJHG · 2020Article
- High-throughput phenotyping reveals expansive genetic and structural underpinnings of immune variation.Nature immunology · 2020Article
- Forward genetic screen in human podocytes identifies diphthamide biosynthesis genes as regulators of adhesion.American journal of physiology. Renal physiology · 2019Article
- DNA methyltransferase inhibition overcomes diphthamide pathway deficiencies underlying CD123-targeted treatment resistance.The Journal of clinical investigation · 2019Article
- Genome-Wide CRISPR Screening Identifies the Tumor Suppressor Candidate OVCA2 As a Determinant of Tolerance to Acetaldehyde.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Genetic Causes of Craniosynostosis: An Update.Molecular syndromology · 2019Review
- The tumor suppressor OVCA1 is a short half-life protein degraded by the ubiquitin-proteasome pathway.Oncology letters · 2019Article
1 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 1 country.
Funding
Abstract
Loss of OVCA1/DPH2L1 correlates with ovarian and breast cancer. To study its in vivo role, we generated Ovca1 mutant alleles in mice. Ovca1 heterozygotes spontaneously develop cancer. Ovca1 mutant mice die during embryonic development and at birth with developmental delay and defects in multiple organ systems. Cell proliferation defects were observed in Ovca1 mutant mouse embryonic fibroblasts (MEFs). p53 deficiency can rescue these Ovca1 mutant MEF proliferation defects and partially rescue Ovca1 mutant embryonic phenotypes. Furthermore, Ovca1; p53 double heterozygotes developed tumors quicker than p53 heterozygotes and with an increased carcinoma incidence. Multiple tumor burden in Ovca1 heterozygotes that were also p53 deficient was significantly higher than in p53 homozygous mutants. These in vivo findings demonstrate that Ovca1 is a tumor suppressor that can modify p53-induced tumorigenesis and suggest that it acts as a positive regulator for cell cycle progression. The close linkage of OVCA1 and p53 on human Chromosome 17 suggests that coordinated loss may be an important mechanism for the evolution of ovarian, breast, and other tumor phenotypes.
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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.