Filamin a (FLNA) is required for cell-cell contact in vascular development and cardiac morphogenesis

Yuanyi Feng, Ming Hui Chen, Ivan P. Moskowitz, Ashley M. Mendonza, Luis Vidali, Fumihiko Nakamura, David J. Kwiatkowski*, Christopher A. Walsh

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

210 Scopus citations


Mutations in the human Filamin A (FLNA) gene disrupt neuronal migration to the cerebral cortex and cause cardiovascular defects. Complete loss of Flna in mice results in embryonic lethality with severe cardiac structural defects involving ventricles, atria, and outflow tracts, as well as widespread aberrant vascular patterning. Despite these widespread developmental defects, migration and motility of many cell types does not appear to be affected. Instead, Flna-null embryos display abnormal epithelial and endothelial organization and aberrant adherens junctions in developing blood vessels, heart, brain, and other tissues. Essential roles for FLNA in intercellular junctions provide a mechanism for the diverse developmental defects seen in patients with FLNA mutations.

Original languageEnglish (US)
Pages (from-to)19836-19841
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number52
StatePublished - Dec 26 2006


  • Adherens junctions
  • Angiogenesis
  • Cardiovascular morphogenesis
  • Neural crest
  • Neuronal migration

ASJC Scopus subject areas

  • General


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