ArticleBlood2007
Lack of endothelial cell survivin causes embryonic defects in angiogenesis, cardiogenesis, and neural tube closure.
Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 81 citations in OpenAlex.
- Elevated survivin expression in peripheral blood mononuclear cells is central to collateral formation in coronary chronic total occlusion.International journal of molecular medicine · 2015Trial
- BIRC5 modulates keratinocyte proliferation and apoptosis via PI3K/AKT/mTOR-mediated autophagy.Scientific reports · 2026Article
- The role of endothelial-derived factors in neural tube development: implications for organoid models.Open biology · 2025Review
- Article
- Functional cargos of exosomes derived from Flk-1Communications biology · 2022Article
- Association of BIRC5 Gene Polymorphism with the Collateral Circulation and Severity of Large Artery Atherosclerotic Stroke.International journal of clinical practice · 2022Article
- BIRC5 promotes cancer progression and predicts prognosis in laryngeal squamous cell carcinoma.PeerJ · 2022Article
- DEPDC1B regulates the progression of human chordoma through UBE2T-mediated ubiquitination of BIRC5.Cell death & disease · 2021Article
- Inverse and reciprocal regulation of p53/p21 and Bmi-1 modulates vasculogenic differentiation of dental pulp stem cells.Cell death & disease · 2021Article
- Contribution of cell death signaling to blood vessel formation.Cellular and molecular life sciences : CMLS · 2021Review
- The protection effects of survivin in the cell model of CVB3-induced viral myocarditis.Heart and vessels · 2020Article
- Article
- Article
- Roles of ErbB3-binding protein 1 (EBP1) in embryonic development and gene-silencing control.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Potential Involvement ofOxidative medicine and cellular longevity · 2019Article
- Antiapoptotic Molecule Survivin in Transplantation: Helpful or Harmful?Journal of transplantation · 2018Review
- Article
- Influence of survivin-targeted therapy on chemosensitivity in the treatment of acute myeloid leukemia.Cancer letters · 2015Article
- Loss of β2-spectrin prevents cardiomyocyte differentiation and heart development.Cardiovascular research · 2014Article
- Regulation of angiogenesis via Notch signaling in breast cancer and cancer stem cells.Biochimica et biophysica acta · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 6 institutions in 5 countries.
Funding
Abstract
We explored the physiologic role of endothelial cell apoptosis during development by generating mouse embryos lacking the inhibitor of apoptosis protein (IAP) survivin in endothelium. This was accomplished by intercrossing survivin(lox/lox) mice with mice expressing cre recombinase under the control of the endothelial cell specific tie1 promoter (tie1-cre mice). Lack of endothelial cell survivin resulted in embryonic lethality. Mutant embryos had prominent and diffuse hemorrhages from embryonic day 9.5 (E9.5) and died before E13.5. Heart development was strikingly abnormal. Survivin-null endocardial lineage cells could not support normal epithelial-mesenchymal transformation (EMT), resulting in hypoplastic endocardial cushions and in utero heart failure. In addition, 30% of mutant embryos had neural tube closure defects (NTDs) that were not caused by bleeding or growth retardation, but were likely due to alterations in the release of soluble factors from endothelial cells that otherwise support neural stem cell proliferation and neurulation. Thus, regulation of endothelial cell survival, and maintenance of vascular integrity by survivin are crucial for normal embryonic angiogenesis, cardiogenesis, and neurogenesis.
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.