Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Mutations within the MGC4607 gene cause cerebral cavernous malformations.
CCM1 and CCM2 protein interactions in cell signaling: implications for cerebral cavernous malformations pathogenesis.
CCM3 interacts with CCM2 indicating common pathogenesis for cerebral cavernous malformations.
Regulation of cardiovascular development and integrity by the heart of glass-cerebral cavernous malformation protein pathway.
Crystal structure of CCM3, a cerebral cavernous malformation protein critical for vascular integrity.
Structural basis of the junctional anchorage of the cerebral cavernous malformations complex.
Structural studies of cerebral cavernous malformations 2 (CCM2) reveal a folded helical domain at its C-terminus.
Structural basis for the disruption of the cerebral cavernous malformations 2 (CCM2) interaction with Krev interaction trapped 1 (KRIT1) by disease-associated mutations.
Phospho-tyrosine dependent protein-protein interaction network.
Widespread macromolecular interaction perturbations in human genetic disorders.
A reference map of the human binary protein interactome.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Multimodal cell maps as a foundation for structural and functional genomics.
Rac-MEKK3-MKK3 scaffolding for p38 MAPK activation during hyperosmotic shock.
Cerebral cavernous malformation 2 protein promotes smad ubiquitin regulatory factor 1-mediated RhoA degradation in endothelial cells.
Cerebral cavernous malformations proteins inhibit Rho kinase to stabilize vascular integrity.
Cerebral cavernous malformations arise from endothelial gain of MEKK3-KLF2/4 signalling.