NYU Dataset
NOGOB Receptor Deficiency Increases Cerebrovascular Permeability and Hemorrhage
UID: 10611
- Description
Cerebral cavernous malformation (CCM) lesions are caused by loss of function of CCM genes. Previous study showed that NOGOB receptor (NGBR) knockout in endothelial cells (ECs) results in cerebrovascular lesions in the mouse embryo. However, the molecular mechanism by which NGBR regulates CCM1/2 expression has not been explained. This study revealed that genetic depletion of NGBR in ECs results in CCM1/2 expression deficiency and cerebrovascular lesions. This dataset contains RNA sequencing data. The study suggests that modulating NGBR and HBO1-mediated histone acetylation may be an epigenetic regulation related to the pathogenesis of certain types of sporadic CCMs promoted by CCM1/2 deficiency.
NgbrECKO mice
Associated Publications
Data Type
Equipment Used
Software Used
Access
- Restrictions
-
Free to All
- Instructions
- The sequencing data are deposited in the NCBI’s Gene Expression Omnibus (GEO) database.
Agilent Fragment Analyzer System
PerkinElmer Microplate Reader
- Grant Support
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GRNT33671180/American Heart Association
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