ArticleMolecular & cellular proteomics : MCP2014
Novel protein interactions with endoglin and activin receptor-like kinase 1: potential role in vascular networks.
Article in Molecular & cellular proteomics : MCP, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 23 citations in OpenAlex.
- Alpha-cell glucagon is essential for maintaining β-cell function and identity in adult mice.The Journal of biological chemistry · 2026Article
- An update on preclinical models of hereditary haemorrhagic telangiectasia: Insights into disease mechanisms.Frontiers in medicine · 2022Review
- Generation of a Soluble Form of Human Endoglin Fused to Green Fluorescent Protein.International journal of molecular sciences · 2021Article
- Membrane and soluble endoglin role in cardiovascular and metabolic disorders related to metabolic syndrome.Cellular and molecular life sciences : CMLS · 2021Review
- Potential Second-Hits in Hereditary Hemorrhagic Telangiectasia.Journal of clinical medicine · 2020Review
- Endoglin Protein Interactome Profiling Identifies TRIM21 and Galectin-3 as New Binding Partners.Cells · 2019Article
- Endoglin as an Adhesion Molecule in Mature and Progenitor Endothelial Cells: A Function Beyond TGF-β.Frontiers in medicine · 2019Review
- Physical interaction of STAT1 isoforms with TGF-β receptors leads to functional crosstalk between two signaling pathways in epithelial ovarian cancer.Journal of experimental & clinical cancer research : CR · 2018Article
- Fundamentals of protein interaction network mapping.Molecular systems biology · 2015Review
- Molecular chaperone Hsp90 is a therapeutic target for noroviruses.Journal of virology · 2015Article
- Clinicopathological and cellular signature of PAK1 in human bladder cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Complexity of macrophage migration inhibitory factor (MIF) and other angiogenic biomarkers profiling in pulmonary arterial hypertension.Pulmonary circulationArticle
- Systems medicine: evolution of systems biology from bench to bedside.Wiley interdisciplinary reviews. Systems biology and medicineReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 7 institutions in 3 countries.
Funding
Abstract
Endoglin and activin receptor-like kinase 1 are specialized transforming growth factor-beta (TGF-β) superfamily receptors, primarily expressed in endothelial cells. Mutations in the corresponding ENG or ACVRL1 genes lead to hereditary hemorrhagic telangiectasia (HHT1 and HHT2 respectively). To discover proteins interacting with endoglin, ACVRL1 and TGF-β receptor type 2 and involved in TGF-β signaling, we applied LUMIER, a high-throughput mammalian interactome mapping technology. Using stringent criteria, we identified 181 novel unique and shared interactions with ACVRL1, TGF-β receptor type 2, and endoglin, defining potential novel important vascular networks. In particular, the regulatory subunit B-beta of the protein phosphatase PP2A (PPP2R2B) interacted with all three receptors. Interestingly, the PPP2R2B gene lies in an interval in linkage disequilibrium with HHT3, for which the gene remains unidentified. We show that PPP2R2B protein interacts with the ACVRL1/TGFBR2/endoglin complex and recruits PP2A to nitric oxide synthase 3 (NOS3). Endoglin overexpression in endothelial cells inhibits the association of PPP2R2B with NOS3, whereas endoglin-deficient cells show enhanced PP2A-NOS3 interaction and lower levels of endogenous NOS3 Serine 1177 phosphorylation. Our data suggest that endoglin regulates NOS3 activation status by regulating PPP2R2B access to NOS3, and that PPP2R2B might be the HHT3 gene. Furthermore, endoglin and ACVRL1 contribute to several novel networks, including TGF-β dependent and independent ones, critical for vascular function and potentially defective in HHT.
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.