Connexin 43 gap junctions contribute to brain endothelial barrier hyperpermeability in familial cerebral cavernous malformations type III by modulating tight junction structure-Reference-Cited by-同舟云学术

Connexin 43 gap junctions contribute to brain endothelial barrier hyperpermeability in familial cerebral cavernous malformations type III by modulating tight junction structure

Published:2018-01-02 Issue:5 Volume:32 Page:2615-2629
ISSN:0892-6638
Container-title:The FASEB Journal
language:en
Short-container-title:FASEB j.

Author:

Johnson Allison M.¹,Roach James P.²,Hu Anna¹,Stamatovic Svetlana M.³,Zochowski Michal R.⁴,Keep Richard F.²,Andjelkovic Anuska V.¹

Affiliation:

1. Department of Pathology Medical School University of Michigan Ann Arbor Michigan USA

2. Department of Neurosurgery Medical School University of Michigan Ann Arbor Michigan USA

3. Neuroscience Graduate Program Medical School University of Michigan Ann Arbor Michigan USA

4. Department of Physics and Biophysics University of Michigan Ann Arbor Michigan USA

Funder

National Institutes of Health

National Science Foundation

Publisher

Wiley

Subject

Genetics,Molecular Biology,Biochemistry,Biotechnology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1096/fj.201700699R

Reference44 articles.

1. Vascular Permeability in Cerebral Cavernous Malformations

2. A PP2A Phosphatase High Density Interaction Network Identifies a Novel Striatin-interacting Phosphatase and Kinase Complex Linked to the Cerebral Cavernous Malformation 3 (CCM3) Protein

3. STRIPAK complexes: Structure, biological function, and involvement in human diseases

4. PDCD10 (CCM3) regulates brain endothelial barrier integrity in cerebral cavernous malformation type 3: role of CCM3-ERK1/2-cortactin cross-talk

5. A novel mouse model of cerebral cavernous malformations based on the two-hit mutation hypothesis recapitulates the human disease

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