ArticleScientific reports2016
Extraembryonic but not embryonic SUMO-specific protease 2 is required for heart development.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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
24 citing papers in PubMed.
- Mouse Trophoblast Stem Cells Are Deficient in TNFα-Activated NFκB Signaling Pathway and Inflammatory Response.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Article
- The placental effects of trisomy for human chromosome 21 orthologs in four mouse models of Down syndrome.Biology open · 2025Article
- Interdependence of placenta and fetal cardiac development.Prenatal diagnosis · 2024Review
- PIBF1 regulates trophoblast syncytialization and promotes cardiovascular development.Nature communications · 2024Article
- Mouse Trophoblast Cells Have Attenuated Responses to TNF-α and IFN-γ and Can Avoid Synergic Cytotoxicity of the Two Cytokines.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- The Trophoblast Compartment Helps Maintain Embryonic Pluripotency and Delays Differentiation towards Cardiomyocytes.International journal of molecular sciences · 2023Article
- SENP2 restrains the generation of pathogenic Th17 cells in mouse models of colitis.Communications biology · 2023Article
- Defects in placental syncytiotrophoblast cells are a common cause of developmental heart disease.Nature communications · 2023Article
- Mouse Trophoblast Cells Can Provide IFN-Based Antiviral Protection to Embryonic Stem Cells via Paracrine Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Inefficient development of syncytiotrophoblasts in theProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Protein sumoylation in normal and cancer stem cells.Frontiers in molecular biosciences · 2022Review
- SUMO-specific Isopeptidases Tuning Cardiac SUMOylation in Health and Disease.Frontiers in molecular biosciences · 2021Review
- The role of SUMOylation during development.Biochemical Society transactions · 2020Review
- Forebrain excitatory neuron-specific SENP2 knockout mouse displays hyperactivity, impaired learning and memory, and anxiolytic-like behavior.Molecular brain · 2020Article
- The requirement of SUMO2/3 for SENP2 mediated extraembryonic and embryonic development.Developmental dynamics : an official publication of the American Association of Anatomists · 2020Article
- Zinc deficiency induces abnormal development of the myocardium by promoting SENP5 overexpression.PloS one · 2020Article
- Phases and Mechanisms of Embryonic Cardiomyocyte Proliferation and Ventricular Wall Morphogenesis.Pediatric cardiology · 2019Review
- Secondary Placental Defects inFrontiers in physiology · 2019Article
- Article
- Near to One's Heart: The Intimate Relationship Between the Placenta and Fetal Heart.Frontiers in physiology · 2018Review
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.
Funding
Abstract
SUMO-specific protease 2 (SENP2) activities to remove SUMO from its substrates is essential for development of trophoblast stem cells, niches and lineages. Global deletion of SENP2 leads to midgestation lethality, and causes severe defects in the placenta which is accompanied by embryonic brain and heart abnormalities. Because of the placental deficiencies, the role of SENP2 in development of the embryonic tissues has not been properly determined. The brain and heart abnormalities may be secondary to placental insufficiency. Here we have created a new mouse strain permitting conditional inactivation of SENP2. Mice homozygous for germline deletion of the conditional allele exhibit trophoblast defects and embryonic abnormalities resembling the global SENP2 knockout. However, tissue-specific disruptions of SENP2 demonstrate its dispensable role in embryogenesis. Placental expression of SENP2 is necessary and sufficient for embryonic heart and brain development. Using a protease deficient model, we further demonstrate the requirement of SENP2-dependent SUMO modification in development of all major trophoblast lineages. SENP2 regulates sumoylation of Mdm2 which controls p53 activities critical for G-S transition of mitotic division and endoreduplication in trophoblast proliferation and differentiation, respectively. The differentiation of trophoblasts is also dependent on SENP2-mediated activation of p57(Kip2), a CDK-specific inhibitor required for endoreduplication.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.