Long QT syndrome type 1 (Q85868): Difference between revisions

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LQT1 é o tipo mais comum de síndrome do QT longo, representando cerca de 30 a 35 por cento de todos os casos. O gene LQT1 é o KCNQ1, que foi isolado no cromossomo 11p15.5. KCNQ1 codifica o canal de potássio controlado por voltagem KvLQT1 que é altamente expresso no coração. Acredita-se que o produto do gene KCNQ1 produza uma subunidade alfa que interage com outras proteínas (em particular, a subunidade beta minK) para criar o canal iônico IKs, que é responsável pela corrente retificadora de potássio atrasada do potencial de ação cardíaco.
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LQT1 is the most common type of long QT syndrome, making up about 30 to 35 percent of all cases. The LQT1 gene is KCNQ1, which has been isolated to chromosome 11p15.5. KCNQ1 codes for the voltage-gated potassium channel KvLQT1 that is highly expressed in the heart. It is believed that the product of the KCNQ1 gene produces an alpha subunit that interacts with other proteins (in particular, the minK beta subunit) to create the IKs ion channel, which is responsible for the delayed potassium rectifier current of the cardiac action potential.

Revision as of 11:13, 15 August 2026

LQT1 is the most common type of long QT syndrome, making up about 30 to 35 percent of all cases. The LQT1 gene is KCNQ1, which has been isolated to chromosome 11p15.5. KCNQ1 codes for the voltage-gated potassium channel KvLQT1 that is highly expressed in the heart. It is believed that the product of the KCNQ1 gene produces an alpha subunit that interacts with other proteins (in particular, the minK beta subunit) to create the IKs ion channel, which is responsible for the delayed potassium rectifier current of the cardiac action potential.
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    Long QT syndrome type 1
    LQT1 is the most common type of long QT syndrome, making up about 30 to 35 percent of all cases. The LQT1 gene is KCNQ1, which has been isolated to chromosome 11p15.5. KCNQ1 codes for the voltage-gated potassium channel KvLQT1 that is highly expressed in the heart. It is believed that the product of the KCNQ1 gene produces an alpha subunit that interacts with other proteins (in particular, the minK beta subunit) to create the IKs ion channel, which is responsible for the delayed potassium rectifier current of the cardiac action potential.

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