Our findings support the association of the epistatic interactions of ALOX5AP, THBD, and KNG1 and present novel evidence for the main effect of KNG1 gene on IS susceptibility, suggesting a modulation of stroke risk by a genetic main effect and gene-gene interactions.
Genetic polymorphisms of ALOX5AP and CYP3A5 increase susceptibility to ischemic stroke and are associated with atherothrombotic events in stroke patients.
Using a case-control design, the whole coding and adjoining intronic regions of ALOX5AP were sequenced to study the role of SNPs and their interplay with other risk factors in Greek patients with stroke.
Genetic variation in members of the leukotriene biosynthesis pathway confer an increased risk of ischemic stroke: a replication study in two independent populations.
However, genetic association studies that have examined the association between ALOX5AP gene variants (HapA haplotype, HapB haplotype, and SG polymorphisms) and stroke have produced conflicting results.
Genetic variation in the genes ALOX5AP (arachidonate 5-lipoxygenase-activating protein) and LTA4H (leukotriene A4 hydrolase) has previously been shown to contribute to the risk of MI (myocardial infarction) and stroke in Icelandic and Scottish populations.
Genetic variation in the gene ALOX5AP, encoding arachidonate 5-lipoxygenase-activating protein, have been suggested to increase risk for myocardial infarction and stroke.
Eight variants in five candidate genes were examined for the risk of stroke, including the SG13S32 (rs9551963), SG13S42 (rs4769060), SG13S89 (rs4769874), and SG13S114 (rs10507391) variants of the 5-lipoxygenase activating protein (ALOX5AP) gene, the G860A (rs751141) variant of the soluble epoxide hydrolase (EPHX2) gene, the rs1057910" genes_norm="1559">A1075C (rs1057910) variant of the CYP2C9*2 gene, the rs1799853" genes_norm="1559;240">C430T (rs1799853) variant of the CYP2C9*3 gene, and the A6986G (rs776746) variant of the CYP3A5 gene.
In atherothrombotic and small-artery disease subtypes, none of the seven SNPs was associated with any stroke risk; however, the ALOX5AP gene might be related to ischemic stroke incidence in females.
Previous studies have implicated that two at-risk haplotypes (HapA and HapB) of gene-encoding 5-lipoxygenase-activating protein (ALOX5AP) were significantly associated with stroke.
We conclude that variants of ALOX5AP are involved in the pathogenesis of both myocardial infarction and stroke by increasing leukotriene production and inflammation in the arterial wall.
5-lipoxygenase activating (ALOX5AP) gene involved in the synthesis of leukotrienes, has been recognized as an important gene contributing towards susceptibility of stroke risk.
Recently, the 5-lipoxygenase activating protein gene (ALOX5AP) was reported to confer a risk of myocardial infarction (MI) and stroke, independent of conventional risk factors.
We conclude that variants of ALOX5AP are involved in the pathogenesis of both myocardial infarction and stroke by increasing leukotriene production and inflammation in the arterial wall.
A nominally significant association with stroke was observed with several SNPs from ALOX5AP, including SNP SG13S114, which had been part of the Icelandic at-risk haplotype.
Recent findings have implicated specific gene polymorphisms of arachidonate 5-lipoxygenase-activating protein (ALOX5AP), and 2 at-risk haplotypes (HapA, HapB) in myocardial infarction and stroke.
The effect of activating 5-lipoxygenase (ALOX5AP) gene polymorphisms on stroke risk may be influenced by the coexistence of modifiable predisposing conditions.
Studies that employ genome-wide linkage scans with hundreds of small nuclear families have identified new susceptibility genes for coronary artery disease and myocardiaI infarction, including ALOX5AP (encoding 5-lipoxygenase-activating protein) associated with myocardial infarction and stroke and PDE4D (encoding phosphodiesterase 4D) for ischemic stroke.