Expression and transcriptional control of human KCNE genes (Q28283081)

1

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Candice L Turner

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Leomar Y Ballester

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Alfred L George

Phylogeny of ion channels: clues to structure and function

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language of work or name

English

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publication date

January 2006

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published in

Genomics

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volume

87

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issue

1

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page(s)

119-28

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cites work

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Do all voltage-gated potassium channels use MiRPs?

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Coassembly of K(V)LQT1 and minK (IsK) proteins to form cardiac I(Ks) potassium channel

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K(V)LQT1 and lsK (minK) proteins associate to form the I(Ks) cardiac potassium current

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KCNE2 confers background current characteristics to the cardiac KCNQ1 potassium channel

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A constitutively open potassium channel formed by KCNQ1 and KCNE3

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KCNE4 is an inhibitory subunit to the KCNQ1 channel

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KCNE5 induces time- and voltage-dependent modulation of the KCNQ1 current

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Expression of multiple KCNE genes in human heart may enable variable modulation of I(Ks).

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Mutations in the hminK gene cause long QT syndrome and suppress IKs function

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Spectrum of mutations in long-QT syndrome genes. KVLQT1, HERG, SCN5A, KCNE1, and KCNE2

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MiRP1 forms IKr potassium channels with HERG and is associated with cardiac arrhythmia

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Identification and functional characterization of a novel KCNE2 (MiRP1) mutation that alters HERG channel kinetics

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MiRP2 forms potassium channels in skeletal muscle with Kv3.4 and is associated with periodic paralysis

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A minK-HERG complex regulates the cardiac potassium current I(Kr)

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Modulation of Kv4.3 current by accessory subunits

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KCNE2 modulates current amplitudes and activation kinetics of HCN4: influence of KCNE family members on HCN4 currents.

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KCNE4 is an inhibitory subunit to Kv1.1 and Kv1.3 potassium channels

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Molecular basis of species-specific expression of repolarizing K+ currents in the heart.

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Genomic structure of three long QT syndrome genes: KVLQT1, HERG, and KCNE1.

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