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Article

Cerebral cavernous malformations proteins inhibit Rho kinase to stabilize vascular integrity.

The Journal of experimental medicine - 12 Apr 2010

Stockton Rebecca A, Shenkar Robert, Awad Issam A, Ginsberg Mark H

Abstract excerpt

Endothelial cell-cell junctions regulate vascular permeability, vasculogenesis, and angiogenesis. Familial cerebral cavernous malformations (CCMs) in humans result from mutations of CCM2 (malcavernin, OSM, MGC4607), PDCD10 (CCM3), or KRIT1 (CCM1), a Rap1 effector which stabilizes endothelial cell-cell junctions. Homozygous loss of KRIT1 or CCM2 produces lethal vascular phenotypes in mice and zebrafish. We report...

Topics

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
Animal Structures
Animals
Brain Edema
Capillary Permeability
Carrier Proteins
Edema, Cardiac
Endothelial Cells
Endothelium, Vascular
Hemangioma, Cavernous, Central Nervous System

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Humans

KRIT1 Protein

Mice

Mice, Inbred C57BL

Mice, Mutant Strains

Microfilament Proteins

Microtubule-Associated Proteins

Mutation

Source

Open in PubMed Open full text

Identifiers

PMID: 20308363
DOI: 10.1084/jem.20091258
PMCID: PMC2856024

Genes

CCM2
OSM
PDCD10

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-20308363-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 29 Aug 2026.

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