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Article

Loss of CCM3 impairs DLL4-Notch signalling: implication in endothelial angiogenesis and in inherited cerebral cavernous malformations.

Journal of cellular and molecular medicine - 1 Mar 2013

You Chao, Sandalcioglu Ibrahim Erol, Dammann Philipp, Felbor Ute, Sure Ulrich, Zhu Yuan

Abstract excerpt

CCM3, a product of the cerebral cavernous malformation 3 or programmed cell death 10 gene (CCM3/PDCD10), is broadly expressed throughout development in both vertebrates and invertebrates. Increasing evidence indicates a crucial role of CCM3 in vascular development and in regulation of angiogenesis and apoptosis. Furthermore, loss of CCM3 causes inherited (familial) cerebral cavernous malformation (CCM), a common...

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Topics

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Share to Apoptosis Regulatory Proteins
Share to Basic Helix-Loop-Helix Transcription Factors

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Endothelium, Vascular

Share to Hemangioma, Cavernous, Central Nervous System

Share to Neovascularization, Pathologic

Share to Receptor, Notch4

Share to Receptors, Notch

Share to Transcription Factor HES-1

Source

Open in PubMed Open full text

Identifiers

PMID: 23388056
DOI: 10.1111/jcmm.12022
PMCID: PMC3823022

Genes

DLL4
HES1
HEY2
PDCD10

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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