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Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Additionally we are shipping and many more products for this protein.
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Data show that voltage-gated potassium channel (show KCNQ1 Antibodies) KCNE3 directly affects the S4 movement in potassium channel (show KCNAB2 Antibodies) KCNQ1 (show KCNQ1 Antibodies).
KCNQ1 (show KCNQ1 Antibodies)/KCNE3 channels make only a small contribution to basolateral conductance in normal colonic crypts, with increased channel activity in UC appearing insufficient to prevent colonic cell depolarization in this disease.
KCNE1 (show KCNE1 Antibodies) and KCNE3: The yin and yang of voltage-gated K(+) channel (show KCND3 Antibodies) regulation
A KCNE3 T4A (show MAK10 Antibodies) mutation was identified in a Japanese patient presenting Brugada-pattern ECG and neurally mediated syncope.
Allele frequencies are studied for 11 known variants of KCNE3 gene, of which two (F66F and R83H) are polymorphic but are not associated with chronic tinnitus.
The results of this study indicated that Kv7.5 (show KCNQ5 Antibodies) contributes to the spatial regulation.
2 of the 8 MiRP2 extracellular domain acidic residues (D54 (show TPD52L2 Antibodies) and D55) are important for KCNQ1 (show KCNQ1 Antibodies)-MiRP2 constitutive activation.
data show that SNPs in KCNE1 (show KCNE1 Antibodies) and KCNE3 are not associated with Meniere disease in Caucasians
The KCNE3 protein within the micellesis in monomeric form and acquires mainly alpha-helical conformation.
Ectopic expression of KCNE3 accelerates cardiac repolarization and abbreviates the QT interval.
This study showed that Kcne3 deletion impairs muscle strength and flexibility in mice.
Null deletion of Kcne3 produces profound changes in the excitability of auditory neurons.
Kcne3 deletion is therefore arrhythmogenic by a novel mechanism in which secondary hyperaldosteronism, associated with an adrenal-specific lymphocyte infiltration, impairs ventricular repolarization.
Data suggest that because the abundance and subcellular localization of KCNQ1 (show KCNQ1 Antibodies) was unchanged in kcne3(-/-) mice, the modification of biophysical properties of KCNQ1 (show KCNQ1 Antibodies) by KCNE3 is essential for its role in intestinal and tracheal transport.
Suggest that KCNE1 (show KCNE1 Antibodies) stabilizes KCNQ1 (show KCNQ1 Antibodies) S4 segment in the resting state and slows the rate of transition to the active state, while KCNE3 stabilizes the S4 segment in the active state.
these data indicate that KCNE1 (show KCNE1 Antibodies) and KCNE3 interact directly with Kv12.2 (show Kcnh3 Antibodies) channels to regulate channel membrane trafficking
Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. This gene encodes a member of the potassium channel, voltage-gated, isk-related subfamily. This member is a type I membrane protein, and a beta subunit that assembles with a potassium channel alpha-subunit to modulate the gating kinetics and enhance stability of the multimeric complex. This gene is prominently expressed in the kidney. A missense mutation in this gene is associated with hypokalemic periodic paralysis.
potassium voltage-gated channel, Isk-related family, member 3
, cardiac voltage-gated potassium channel accessory subunit
, minK-related peptide 2
, minimum potassium ion channel-related peptide 2
, potassium channel subunit beta MiRP2
, potassium voltage-gated channel subfamily E member 3
, voltage-gated K+ channel subunit MIRP2
, mink-related peptide 2
, potassium voltage-gated channel, Isk-related subfamily, gene 3
, potassium voltage-gated channel, Isk-related subfamily, member 3