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Cedars-Sinai study identifies heart-specific protein that protects against arrhythmia
Date:5/18/2014

hin each heart cell changes the genetic 'signaling' changes and the cell gets the message to make less BIN1."

Shaw said cardiologists now use ultrasound images and estimates of the amount of blood pumped out of the left ventricle with each heartbeat to gauge the health of a patient's heart, but cardiologists long have known that this 'ejection fraction' is a poor indicator of patient well-being or outcome.

"The membranes of heart cells, like other cells, recycle, and thus heart cell membranes and their associated BIN1 gets into the bloodstream. By taking a simple blood sample, we can measure what's going on in the heart. As we refine this BIN1 blood test, we believe we will be able to do a biochemical assessment of the heart cell, the myocyte," Shaw said.

Shaw and his team identified the cardiac version of BIN1, but other variations affect other parts of the body. In the brain, for example, it is associated with Alzheimer's disease; in skeletal muscle, BIN1 loss is involved in muscular dystrophy. Slight differences in the BIN1 protein occur within genetic building blocks called exons, and the cardiac version has a signature that includes exons 13 and 17. The research team found that the binding of these two particular building blocks to the myocyte's internal structural proteins creates the cardiac membrane microfolds.


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Contact: Sally Stewart
sally.stewart@cshs.org
310-248-6566
Cedars-Sinai Medical Center
Source:Eurekalert

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