anti-Potassium Voltage-Gated Channel, Shaker-Related Subfamily, Member 5 (KCNA5) Antibodies

Human Potassium Voltage-Gated Channel, Shaker-Related Subfamily, Member 5 (KCNA5) interaction partners

1. Verapamil acts as an open-channel blocker of hKv1.5 channel, presumably due to direct binding to specific amino acids within pore region of hKv1.5 channel, such as Thr479, Thr480, Val505, Ile508, Val512 and Val516.

2. The N terminus and transmembrane segment S1 of Kv1.5 can co-assemble with the rest of the channel independently of the S1-S2 linkage.

3. Molecular dynamics simulations are employed to determine the inhibitory mechanisms of three drugs, 5-(4-phenoxybutoxy)psoralen (PAP-1), vernakalant, and flecainide, on the voltage-gated K(+) channel Kv1.5, a target for the treatment of cardiac arrhythmia.

4. This study adds insights to the functional impact of KCNA5 mutations in modulating atrial contractile functions.

5. In addition, as IKur is an atrial-specific channel and a number of IKur-selective blockers have been developed as anti-AF agents, this study also helps to understand some contradictory results on both pro- and anti-arrhythmic effects of blocking IKur.

6. our finding indicated that KCNA5 protein may interact with Cav-1, thereby contributing to the proliferation and early transformation of mammary cells.

7. Putative binding sites for arachidonic acid on the human cardiac Kv 1.5 channel

8. Studies demonstrate that DNA hypermethylation contributes to epigenetic repression of the KCNA5 locus and that the resulting suppression of the Kv1.5 ion channel supports cancer cell proliferation.

9. Kv1.5 expression is increased in osteosarcoma cells and tissues and shRNA mediated silencing of Kv1.5 results in cell proliferation inhibition, cell cycle arrest, and induces cell apoptosis.

10. Direct interaction with specific amino acids underlies the blocking action of propofol on voltage-gated hKv1.5 channel.

11. demonstrate that PK treatment cleaved mature membrane-bound (75kDa) Kv1.5 channels at a single locus in the S1-S2 linker, producing 42-kDa N-terminal fragments and 33-kDa C-terminal fragments

12. These results indicate that CHIP decreases the Kv1.5 protein level and functional channel by facilitating its degradation in concert with chaperone Hsc70

13. The expression of Kv1.5 channel protein changes with atrial fibrillation but not with age, rheumatic heart diseases, and sex in atrial fibrillation.

14. One KCNA5 variant, H463R, was a novel mutation; the histidine at codon 463 is located in the S5-pore loop, in the vicinity of the pore of KV1.5 subunit. The other variant, T527M, showed a gain-of-function effect with an enhanced steady-state activation.

15. The KCNA5 promoter is marked in cancer cells with PcG-dependent chromatin repressive modifications that increase in hypoxia.

16. Mutations in KCNA5 gene is not associated with pulmonary arterial hypertension.

17. Protein kinase C inhibition results in a Kv 1.5 and Kv beta 1.3 pharmacology closer to Kv 1.5 channels

18. Data do not indicate an important role of potassium voltage-gated channel shaker-related subfamily member 5 (KCNA5) as a sclerosis (SSc)-susceptibility factor or as a pulmonary arterial hypertension (PAH)-development genetic marker for SSc patients.

19. isoform betaII plays a central role in the PKC-dependent regulation of Kv1.5/Kvbeta1.2 channels.

20. These results indicate that low temperature exposure stabilizes the protein in the cellular organelles or on the plasma membrane, and modulates its maturation and trafficking, thus enhancing the currents of hKv1.5 and its trafficking defect mutants.

Mouse (Murine) Potassium Voltage-Gated Channel, Shaker-Related Subfamily, Member 5 (KCNA5) interaction partners

1. KV1.5 channels predominantly associate with KVbeta1 and KVbeta2 proteins and that KVbeta2 performs a chaperone function for KV1.5 channels in arterial myocytes, thereby facilitating Kv1alpha trafficking and membrane localization.

2. The findings uncover detailed molecular mechanisms underpinning a channelopathy-linked form of atrial fibrillation and emphasize the inevitability of considering extracardiac mechanisms in genetic arrhythmia syndromes.

3. Silencing of Kv1.5 improved endothelium-dependent vasodilatation in thoracic aorta from type 2 diabetes mice.

4. Intracellular urate taken up by UATs enhanced Kv1.5 protein expression and function in HL-1 atrial myocytes.

5. JAK3 contributes to the regulation of membrane Kv1.5 protein abundance and activity, an effect sensitive to ouabain and thus possibly involving Na(+)/K(+) ATPase activity.

6. KV1.5, a DPO-1-sensitive KDR channel, plays a major role in determining microvascular tone and the response to vasoconstrictors and vasodilators.

7. Kv1.5 channels in vascular smooth muscle play a critical role in coupling myocardial blood flow to cardiac metabolism.

8. the Kv1.5 subunit has a role in electrical remodeling of preoptic GABAergic neurons

9. MYO5A and MYO5B control functionally distinct steps in the surface trafficking of Kv1.5.

10. e-LXA4 promoted a modest upregulation of Kv1.5 mRNA that was suppressed by LPS or IL-4/IL-13.

11. The combined down-regulation of Kv4.2, Kv1.5 and KChIP2 prior to the onset of HF may play an important role in the premature sudden death in this DCM model.

12. cortactin was required for N-cadherin-mediated enhancement of Kv1.5 channel activity

13. Data confirm KCNA5 in left/right atria & indicate functional interaction of KCNA5 (ultra rapid) & KCNH2 (rapid). Action potentials are longer in right atrial myocytes than in left; this is due partly to smaller amplitude of KCNA5 in right atrium.

14. KChIP2 contributes to the formation of functional mouse ventricular Kv1.5 channels

15. hyperthyroidism resulted in more significant action potential shortening and greater delayed rectifier K(+) current increases in the right vs. the left atrium, which can contribute to the propensity for atrial arrhythmia in hyperthyroid heart

16. Kv1.5 co-associates with Kv1.3, generating functional heterotetramers in macrophages

17. Kv1.3-based treatments to alter physiological responses, such as proliferation and activation, are impaired by Kv1.5 expression

18. Our results show that Kcna5 promoter activity in vascular smooth muscle is critically dependent on Sp1 regulation via CACCC box motifs and identify mechanisms that potentially influence the expression of K(V)1.5 channel expression.

19. Kv1.5 has a role in Rab-GTPase-dependent endocytic recycling in atrial myocytes

20. These results suggest that the inhibition of K(v) channel expression and rise in [Ca(2+)](i) during chronic hypoxia may be the result of HIF-1-dependent induction of ET-1.