Abstract:
:The rapid (IKr) and slow (IKs) delayed rectifier K+ currents are key regulators of cardiac repolarization. HERG encodes the Kr channel, and KVLQT1 and hminK encode subunits that coassemble to form Ks channels. Mutations in any one of these genes cause Romano-Ward syndrome, an autosomal dominant form of long QT syndrome (LQT). Mutations in KVLQT1 and HERG are the most common cause of LQT. Not all missense mutations of HERG or KVLQT1 have the same effect on K+ channel function. Most mutations result in a dominant-negative effect, but the severity of the resulting phenotype varies widely, as judged by reduction of current induced by coexpression of wild-type and mutant subunits in heterologous expression systems. Mutations in hminK (S74L, D76N) reduce IKs by shifting the voltage dependence of activation and accelerating channel deactivation. A recessive form of LQT is caused by mutations in either KVLQT1 or hminK. The functional consequences of mutations in delayed rectifier K+ channel subunits are delayed cardiac repolarization, lengthened QT interval, and an increased risk of torsade de pointes and sudden death.
journal_name
Ann N Y Acad Scijournal_title
Annals of the New York Academy of Sciencesauthors
Sanguinetti MCdoi
10.1111/j.1749-6632.1999.tb11302.xsubject
Has Abstractpub_date
1999-04-30 00:00:00pages
406-13eissn
0077-8923issn
1749-6632journal_volume
868pub_type
杂志文章,评审abstract::In this review, we present (1) the scientific basis for the use of high-dose immunosuppression followed by autologous peripheral blood hematopoietic stem cell transplantation for newly diagnosed type 1 diabetes (T1D); (2) an update of the clinical and laboratory outcome of 20 patients transplanted at the University Ho...
journal_title:Annals of the New York Academy of Sciences
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journal_title:Annals of the New York Academy of Sciences
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journal_title:Annals of the New York Academy of Sciences
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journal_title:Annals of the New York Academy of Sciences
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journal_title:Annals of the New York Academy of Sciences
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journal_title:Annals of the New York Academy of Sciences
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更新日期:2000-01-01 00:00:00
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