ArticleThe EMBO journal1999
JunB is essential for mammalian placentation.
Article in The EMBO journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
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Who cites it
95 citing papers in PubMed, 271 citations in OpenAlex.
- The integrated developmental stress response (ISR-DASR) shift reveals a functional transition from cellular to stem cell organismal adaptation.Scientific reports · 2026Article
- AP1 Transcription Factor in the Regulation of the Urokinase Plasminogen Activation System.Biomolecules · 2026Review
- Extracellular Vesicles Alter Trophoblast Function in Pregnancies Complicated by COVID-19.Journal of extracellular vesicles · 2025Article
- Molecular regulators of defective placental and cardiovascular development in fetal growth restriction.Clinical science (London, England : 1979) · 2024Review
- Lineage regulators TFAP2C and NR5A2 function as bipotency activators in totipotent embryos.Nature structural & molecular biology · 2024Article
- Identification of New Markers of Angiogenic Sprouting Using Transcriptomics: New Role for RND3.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Activating mutations in JAK2 and CALR differentially affect intracellular calcium flux in store operated calcium entry.Cell communication and signaling : CCS · 2024Article
- Identification and RT-qPCR Validation of Biomarkers Based on Butyrate Metabolism-Related Genes to Predict Recurrent Miscarriage.Journal of inflammation research · 2024Article
- Depletion of JunB increases adipocyte thermogenic capacity and ameliorates diet-induced insulin resistance.Nature metabolism · 2024Article
- Vascular cell-adhesion molecule 1 (VCAM-1) regulates JunB-mediated IL-8/CXCL1 expression and pathological neovascularization.Communications biology · 2023Article
- A differentiation roadmap of murine placentation at single-cell resolution.Cell discovery · 2023Article
- Article
- JunB: a paradigm for Jun family in immune response and cancer.Frontiers in cellular and infection microbiology · 2023Review
- Integrated multi-omics analyses reveals molecules governing sperm metabolism potentially influence bull fertility.Scientific reports · 2022Article
- Integrative epigenomic and transcriptomic analysis reveals the requirement of JUNB for hematopoietic fate induction.Nature communications · 2022Article
- Gene-selective transcription promotes the inhibition of tissue reparative macrophages by TNF.Life science alliance · 2022Article
- Glucose-6-Phosphate Dehydrogenase, Redox Homeostasis and Embryogenesis.International journal of molecular sciences · 2022Review
- Article
- Molecular mimicry between SARS-CoV-2 and the female reproductive system.American journal of reproductive immunology (New York, N.Y. : 1989) · 2021Article
- The role of leukemia inhibitory factor in pathogenesis of pre-eclampsia: molecular and cell signaling approach.Journal of molecular histology · 2021Review
35 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lack of JunB, an immediate early gene product and member of the AP-1 transcription factor family causes embryonic lethality between E8.5 and E10.0. Although mutant embryos are severely retarded in growth and development, cellular proliferation is apparently not impaired. Retardation and embryonic death are caused by the inability of JunB-deficient embryos to establish proper vascular interactions with the maternal circulation due to multiple defects in extra-embryonic tissues. The onset of the phenotypic defects correlates well with high expression of junB in wild-type extra-embryonic tissues. In trophoblasts, the lack of JunB causes a deregulation of proliferin, matrix metalloproteinase-9 (MMP-9) and urokinase plasminogen activator (uPA) gene expression, resulting in a defective neovascularization of the decidua. As a result of downregulation of the VEGF-receptor 1 (flt-1), blood vessels in the yolk sac mesoderm appeared dilated. Mutant embryos which escape these initial defects finally die from a non-vascularized placental labyrinth. Injection of junB-/- embryonic stem (ES) cells into tetraploid wild-type blastocysts resulted in a partial rescue, in which the ES cell-derived fetuses were no longer growth retarded and displayed a normal placental labyrinth. Therefore, JunB appears to be involved in multiple signaling pathways regulating genes involved in the establishment of a proper feto-maternal circulatory system.
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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.