ReviewJournal of cell science2014
Cerebral cavernous malformation proteins at a glance.
Review in Journal of cell science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 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
74 citing papers in PubMed, 95 citations in OpenAlex.
- Cerebral cavernous malformations: epidemiology, molecular pathogenesis, diagnosis and therapy.Molecular biomedicine · 2026Review
- Intramedullary Spinal Cord Cavernous Angiomas in Familial Cerebral Cavernous Malformations.Genes · 2026Review
- Partial Oculomotor Nerve Palsy Revealing PDCD10-Related Familial Cerebral Cavernous Malformation in a Child.Cureus · 2026Article
- Identification of the adhesion GPCR ADGRL4/ELTD1 as a novel potential prognostic biomarker for cerebral cavernous malformation disease.Molecular medicine (Cambridge, Mass.) · 2026Article
- Dual recruitment of two CCM2 molecules to KRIT1 suppresses KLF4 expression.Nature communications · 2026Article
- Spinal Cavernous Malformations: A Narrative Review.NeuroSci · 2026Review
- Modeling blood-brain barrier formation and cerebral cavernous malformations in human PSC-derived organoids.Cell stem cell · 2024Article
- Cerebral Cavernous Malformation (CCM)-like Vessel Lesion in the AgedExperimental neurobiology · 2023Article
- Endothelial Cell-Pericyte Interactions in the Pathogenesis of Cerebral Cavernous Malformations (CCMs).Cold Spring Harbor perspectives in medicine · 2023Review
- Endothelial Differentiation ofInternational journal of molecular sciences · 2023Article
- Biomarkers derived from CmP signal network in triple negative breast cancers.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2023Review
- The multifacetedGenes & diseases · 2021Review
- Assessing the association of common genetic variants in EPHB4 and RASA1 with phenotype severity in familial cerebral cavernous malformation.Molecular genetics & genomic medicine · 2021Article
- A novel insight into differential expression profiles of sporadic cerebral cavernous malformation patients with different symptoms.Scientific reports · 2021Article
- CCM3 is a gatekeeper in focal adhesions regulating mechanotransduction and YAP/TAZ signalling.Nature cell biology · 2021Article
- Review
- Protein kinase Cα regulates the nucleocytoplasmic shuttling of KRIT1.Journal of cell science · 2021Article
- Genetic syndromes with vascular malformations - update on molecular background and diagnostics.Archives of medical science : AMS · 2021Article
- Epithelial morphogenesis, tubulogenesis and forces in organogenesis.Current topics in developmental biology · 2021Review
- High Levels of Receptor Tyrosine Kinases in CCM3-Deficient Cells Increase Their Susceptibility to Tyrosine Kinase Inhibition.Biomedicines · 2020Article
14 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 1 institution in 1 country.
Funding
Abstract
Loss-of-function mutations in genes encoding KRIT1 (also known as CCM1), CCM2 (also known as OSM and malcavernin) or PDCD10 (also known as CCM3) cause cerebral cavernous malformations (CCMs). These abnormalities are characterized by dilated leaky blood vessels, especially in the neurovasculature, that result in increased risk of stroke, focal neurological defects and seizures. The three CCM proteins can exist in a trimeric complex, and each of these essential multi-domain adaptor proteins also interacts with a range of signaling, cytoskeletal and adaptor proteins, presumably accounting for their roles in a range of basic cellular processes including cell adhesion, migration, polarity and apoptosis. In this Cell Science at a Glance article and the accompanying poster, we provide an overview of current models of CCM protein function focusing on how known protein-protein interactions might contribute to cellular phenotypes and highlighting gaps in our current understanding.
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.