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4 A role for JCAD has been identified in pathological angiogenesis with decrease vascular formation in response to matrigel and decreased tumour growth.
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JCAD has been identified as a novel component of endothelial cell junctions where it is found to co-localize with VE-Cadherin. JCAD is an intrinsically disordered protein with no recognizable functional domains and little homology to other protein families. The function of the 1359-amino-acid protein encoded by JCAD is largely unknown. This indicates that decreased expression of JCAD associated with the rs2487928 allele is protective, 3 leading to the hypothesis that loss of JCAD would result in reduced atherosclerosis burden.
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2 Using the STARNET data set, we identified an expression quantitative trait locus between the protective allele of the lead SNP rs2487928 which was associated with decreased expression of JCAD in both atherosclerotic and atherosclerosis free arterial tissue. 1 This association has been robustly confirmed in subsequent meta-analyses. We have previously identified a locus on chromosome 10 which harbours a single gene, JCAD (Junctional protein associated with Coronary Artery Disease previously KIAA1462). lipid metabolism or inflammation), other GWAS variants implicate genes without a known functional role in CAD pathogenesis, with the potential to reveal new biological mechanisms. In particular, whilst many GWAS variants implicate genes with known or expected roles in processes that are central to our current understanding of CAD pathogenesis (e.g. The post-GWAS challenge is to identify the genes that confer the causative association with the CAD locus and discover the biological mechanisms linking these genes to CAD. Genome-wide association studies (GWAS) have achieved significant progress in identifying, and robustly replicating, common genetic variation that contributes to increased coronary artery disease (CAD) risk. JCAD, Atherosclerosis, Shear stress, Endothelial cells, Kiaa1462 Knock down of JCAD using siRNA in primary human aortic endothelial cells significantly reduced the response to acute onset of flow, as evidenced by reduced phosphorylation of NF-КB, eNOS, and Akt. Loss of Jcad lead to a reduced recovery perfusion in response to hind limb ischaemia, a model of altered in vivo flow. En face analysis revealed a striking reduction in pro-inflammatory adhesion molecules at sites of disturbed flow on the endothelial cell layer of Jcad −/− mice.
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However, Jcad −/− ApoE −/− mice developed significantly less atherosclerosis in the aortic root and the inner curvature of the aortic arch. Loss of Jcad did not affect blood pressure or heart rate. To study the impact of loss of Jcad on atherosclerosis, Jcad −/− mice were crossed to an ApoE −/− background and fed a high-fat diet from 6 to16 weeks of age. The JCAD risk allele identified by GWAS was associated with reduced FMD and reduced endothelial-dependent relaxations. Vascular function was quantified in subjects with CAD by flow-mediated dilatation (FMD) and vasorelaxation responses in isolated blood vessel segments.