Gαq and hyper-phosphorylated ERK expression in Sturge-Weber syndrome leptomeningeal blood vessel endothelial cells

Vasc Med. 2019 Feb;24(1):72-75. doi: 10.1177/1358863X18786068. Epub 2018 Aug 16.

Authors

Rebecca J Wellman¹, Su Bin Cho², Pratibha Singh¹, Miriya Tune¹, Carlos A Pardo^{3

4}, Anne M Comi^{1

4

5}; BVMC Sturge–Weber syndrome Project Workgroup

Affiliations

¹ 1 Department of Neurology & Developmental Medicine, Hugo W Moser Research Institute, Kennedy Krieger Institute, Baltimore, MD, USA.
² 2 Johns Hopkins University, Baltimore, MD, USA.
³ 3 Department of Pathology, Johns Hopkins School of Medicine, Baltimore, MD, USA.
⁴ 4 Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD, USA.
⁵ 5 Department of Pediatrics, Johns Hopkins School of Medicine, Baltimore, MD, USA.

No abstract available

Keywords: ERK; GNAQ; Gαq; Sturge–Weber syndrome; blood vessel; endothelial cells; leptomeninges.

Publication types

Letter
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

MeSH terms

Antigens, CD34 / analysis
Case-Control Studies
Endothelial Cells / enzymology*
Endothelial Cells / pathology
Extracellular Signal-Regulated MAP Kinases / analysis*
GTP-Binding Protein alpha Subunits, Gq-G11 / analysis*
Humans
Meninges / blood supply*
Phosphorylation
Sturge-Weber Syndrome / enzymology*
Sturge-Weber Syndrome / pathology

Substances

Antigens, CD34
GNAQ protein, human
Extracellular Signal-Regulated MAP Kinases
GTP-Binding Protein alpha Subunits, Gq-G11

Grants and funding

U54 NS065705/NS/NINDS NIH HHS/United States