ReviewOpen biology2020
Signalling through cerebral cavernous malformation protein networks.
Review in Open biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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
22 citing papers in PubMed, 40 citations in OpenAlex.
- MicroRNA-21-3p regulation of NADPH oxidase 4 and vascular endothelial growth factor A contributes to hemorrhage in cerebral cavernous malformations.Non-coding RNA research · 2026Article
- Oxygenated 9H-carbazole-3-carbaldehyde scaffolds as cerebral cavernous malformation-relevant protein-protein interaction disruptors of the HEG1-KRIT1 interface.Journal of computer-aided molecular design · 2026Article
- Human stem cell models in cerebral cavernous malformations.Stem cell research & therapy · 2026Review
- Unveiling a Novel Molecular Interaction and Pro-Metastatic Signaling Cascades Driven by KRIT1.International journal of molecular sciences · 2026Article
- Dual recruitment of two CCM2 molecules to KRIT1 suppresses KLF4 expression.Nature communications · 2026Article
- Familial Cerebral Cavernous Malformations: Pathophysiology, Genetics, Biomarkers, and Treatment Perspectives.Journal of neurochemistry · 2026Review
- TLNRD1-CCM2 interaction maintains endothelial actin networks through a KLF2/4-independent mechanism.JVS-vascular science · 2026Article
- Large language models assisted multi-effect variants mining on cerebral cavernous malformation familial whole genome sequencing.Computational and structural biotechnology journal · 2024Article
- TLNRD1 is a CCM complex component and regulates endothelial barrier integrity.The Journal of cell biology · 2024Article
- Current and Future Treatment Options for Cerebral Cavernous Malformations.Stroke (Hoboken, N.J.) · 2024Review
- Role of Rho-Associated Kinase in the Pathophysiology of Cerebral Cavernous Malformations.Neurology. Genetics · 2024Review
- Plxnd1-mediated mechanosensing of blood flow controls the caliber of the Dorsal Aorta via the transcription factor Klf2.bioRxiv : the preprint server for biology · 2024Article
- Potential role of RhoA GTPase regulation in type interferon signaling in systemic lupus erythematosus.Arthritis research & therapy · 2024Article
- Spatial Mechano-Signaling Regulation of GTPases through Non-Degradative Ubiquitination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Article
- NDR kinase tricornered genetically interacts with Ccm3 and metabolic enzymes in Drosophila melanogaster tracheal development.G3 (Bethesda, Md.) · 2023Article
- Release of STK24/25 suppression on MEKK3 signaling in endothelial cells confers cerebral cavernous malformation.JCI insight · 2023Article
- Zinc's Association with the CmPn/CmP Signaling Network in Breast Cancer Tumorigenesis.Biomolecules · 2022Review
- DOCK4 Regulation of Rho GTPases Mediates Pulmonary Vascular Barrier Function.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Editome landscape of CCM-derived endothelial cells.RNA biology · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cerebral cavernous malformations (CCMs) are neurovascular abnormalities characterized by thin, leaky blood vessels resulting in lesions that predispose to haemorrhages, stroke, epilepsy and focal neurological deficits. CCMs arise due to loss-of-function mutations in genes encoding one of three CCM complex proteins, KRIT1, CCM2 or CCM3. These widely expressed, multi-functional adaptor proteins can assemble into a CCM protein complex and (either alone or in complex) modulate signalling pathways that influence cell adhesion, cell contractility, cytoskeletal reorganization and gene expression. Recent advances, including analysis of the structures and interactions of CCM proteins, have allowed substantial progress towards understanding the molecular bases for CCM protein function and how their disruption leads to disease. Here, we review current knowledge of CCM protein signalling with a focus on three pathways which have generated the most interest-the RhoA-ROCK, MEKK3-MEK5-ERK5-KLF2/4 and cell junctional signalling pathways-but also consider ICAP1-β1 integrin and cdc42 signalling. We discuss emerging links between these pathways and the processes that drive disease pathology and highlight important open questions-key among them is the role of subcellular localization in the control of CCM protein activity.
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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.