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Article

Fibronectin rescues aberrant phenotype of endothelial cells lacking either CCM1, CCM2 or CCM3.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology - 1 Jul 2020

Schwefel Konrad, Spiegler Stefanie, Kirchmaier Bettina C, Dellweg Patricia K E, Much Christiane D, Pané-Farré Jan, Strom Tim M, Riedel Katharina, Felbor Ute, Rath Matthias

Abstract excerpt

Loss-of-function variants in CCM1/KRIT1, CCM2, and CCM3/PDCD10 are associated with autosomal dominant cerebral cavernous malformations (CCMs). CRISPR/Cas9-mediated CCM3 inactivation in human endothelial cells (ECs) has been shown to induce profound defects in cell-cell interaction as well as actin cytoskeleton organization. We here show that CCM3 inactivation impairs fibronectin expression and consequently leads...

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PMID: 32515053
DOI: 10.1096/fj.201902888R

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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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