KIF6

KIF6

A gene on chromosome 6p21.2 that encodes a member of the kinesin-like protein family.
References in periodicals archive ?
Initial efforts focused on genetic variants in kinesin family member 6 (KIF6) that appeared to identify patients who received a greater benefit from statins despite equal C-reactive protein and lipid lowering (9, 10); however, subsequent efforts have called these findings into question (11--13).
Polymorphism in KIF6 gene and benefit from statins after acute coronary syndromes: results from the PROVE IT-TIMI 22 study.
No impact of KIF6 genotype on vascular risk and statin response among 18,348 randomized patients in the heart protection study.
KIF6 polymorphism and the efficacy of rosuvastatin in primary prevention.
Matthew Taylor recently discussed the "step backward" that occurred in genetic risk prediction of coronary artery disease with the discovery that variations in the KIF6 gene might not be clinically associated with CAD after all.
Of course, KIF6 is only one of many genetic markers that have been linked to CAD risk.
Matthew Taylor discussed the "step backward" that occurred in genetic risk prediction of coronary artery disease (CAD) with the discovery that variations in the KIF6 gene might not be clinically associated with CAD after all.
A mutated form of the gene, known as KIF6, is linked with a higher chance of developing coronary heart disease, according to three studies published in the Journal of the American College of Cardiology (1/29).
More than 60% of the American population may carry KIF6, based on the combined research on about 30,000 people.
In the past 5 years, several groups have published studies involving large cohorts of patients with CAD that link variants in the kinesinlike protein 6 (KIF6) gene to coronary risk.
As the evidence accumulated for KIF6's role, companies began to look at the development of clinical assays that culminated in a KIF6 genetic-testing assay that was marketed to cardiologists and internists.
Assimes of Stanford (Calif.) University and colleagues and published last month, refutes much of the previous work, seriously calling into question the validity of the KIF6-coronary artery disease link as well as the clinical testing activity that was built around KIF6 (J.