Open AccessVariants of Rab GTPase–Effector Binding Protein-2 Cause Variation in the Collateral Circulation and Severity of Stroke
Author(s) -
Jennifer L. Lucitti,
Robert Sealock,
Brian K. Buckley,
Hua Zhang,
Lin Xiao,
Andrew C. Dudley,
James E. Faber
Publication year - 2016
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/strokeaha.116.014160
Subject(s) - medicine , rab , effector , collateral circulation , stroke (engine) , gtpase , collateral , collateral damage , circulation (fluid dynamics) , cardiology , microbiology and biotechnology , immunology , biology , mechanical engineering , physics , criminology , finance , sociology , economics , engineering , thermodynamics
The extent (number and diameter) of collateral vessels varies widely and is a major determinant, along with arteriogenesis (collateral remodeling), of variation in severity of tissue injury after large artery occlusion. Differences in genetic background underlie the majority of the variation in collateral extent in mice, through alterations in collaterogenesis (embryonic collateral formation). In brain and other tissues, ≈80% of the variation in collateral extent among different mouse strains has been linked to a region on chromosome 7. We recently used congenic (CNG) fine mapping of C57BL/6 (B6, high extent) and BALB/cByJ (BC, low extent) mice to narrow the region to a 737 Kb locus, Dce1. Herein, we report the causal gene.
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