anti-Potassium Voltage-Gated Channel, Shaker-Related Subfamily, Member 3 (KCNA3) Antibodies

Human Potassium Voltage-Gated Channel, Shaker-Related Subfamily, Member 3 (KCNA3) interaction partners

1. T-cell dependency on Kv1.3 or KCa3.1 might be irreversibly modulated by antigen exposure.

2. In this work, we showed that although both Kv1.1 and Kv1.3 channels are expressed in U87 (glioblastoma), MDA-MB-231 (breast cancer) and LS174 (colon adenocarcinoma) cells, these respond differently to KAaH1 or KAaH2, two homologous Kv1 blockers from scorpion venom

3. Kv1.3 methylation may serve as diagnostic and prognostic markers in colorectal cancer.

4. the tertiary structure of the C-terminal domain of Kv1.3 is necessary and sufficient for Kv1.3- KCNE4 interaction.

5. results identify a caveolin-binding domain in Kv1 channels and highlight the mechanisms that govern the regulation of channel surface localization during cellular processes

6. we report that Kv1.3-NPs reduced NFAT activation and CD40L expression exclusively in CD45RO(+) T cells. Furthermore, Kv1.3-NPs suppressed cytokine release and induced a phenotype switch of T cells from predominantly memory to naive.

7. The implication of Kv1.3 in a wide repertoire of human pathologies indicates this channel is an important therapeutic target.

8. Results contribute to the characterization of leukemic B cells, as it shows that upregulation of Kv1.3 in pathologic B lymphocytes is linked to the oncogenic B-RAF signaling.

9. Data suggest that C-terminus is necessary for Kv1.3-induced cell proliferation; the mechanism involves accessibility of key docking sites at the C terminus; phosphorylation of Tyr-447 by MAP kinase signal cascade appears crucial.

10. concluded that Kv1.3 may stimulate macrophage migration through the activation of ERK.

11. The inhibition of Kv1.3 channels might be involved in antiproliferative and proapoptotic effects of the compounds observed in cancer cell lines expressing these channels.

12. Kv1.3 channels modulate human vascular smooth muscle cells proliferation independently of mTOR signaling pathway.

13. actin dynamics regulates the membrane motility of Kv1.3 channels.

14. The increment and decrement of the basic residue number in a positively charged S4 sensor of Kv1.3 channel yields conductance-voltage relationship curves in the positive direction by approximately 31.2 mV and 2-4 mV

15. the association between Kv1.3 and the COPII cargo adaptor subunit isoform Sec24a

16. Findings reveal that alpha-defensins are endogenous inhibitors of potassium voltage-gated channel subfamily A member 3 (Kv1.3) with distinct interaction mechanisms.

17. JAK2 participates in the signalling, regulating the voltage-gated K(+) channel KCNA3.

18. This study demonstrated that Potassium channel Kv1.3 is highly expressed by microglia in human Alzheimer's disease.

19. These results demonstrate that Kv1.3 channels are primarily localized in the nucleus of several types of cancer cells and human brain tissues where they are capable of regulating nuclear membrane potential and activation of transcription factors

20. the small molecule Kv1.3 blocker PAP-1 dose-dependently inhibited proliferation and suppressed IL-2 and IFN-gamma production.

Mouse (Murine) Potassium Voltage-Gated Channel, Shaker-Related Subfamily, Member 3 (KCNA3) interaction partners

1. Using microglia acutely isolated from adult brains, authors detected Kv1.3 and Kir2.1 currents, and found that intracerebroventricular injection of lipopolysaccharides (LPS) increased the current density and RNA expression of Kv1.3 but did not affect those of Kir2.1. Genetic knockout of Kv1.3 abolished LPS-induced microglial activation exemplified by Iba-1 immunoreactivity and expression of pro-inflammatory mediators.

2. Our data shed light on the putative role of Kv1.3 in weight gain and insulin-dependent responses contributing to knowledge about adipocyte physiology

3. Data show that cereblon (CRBN) limits CD4(+) T-cell activation via epigenetic regulation of Kv1.3 potassium channel (Kv1.3) expression.

4. Following differentiation with LPS or a combination of LPS and IFN-gamma microglia exhibited high KV 1.3 current densities ( approximately 50 pA/pF at 40 mV) and virtually no KCa 3.1 and Kir currents, while microglia differentiated with IL-4 exhibited large Kir 2.1 currents ( approximately 10 pA/pF at -120 mV). KCa 3.1 currents were generally low

5. These studies reveal unexpected roles of Kv1.3 subunit-containing channels in the regulation of firing patterns of striatal cholinergic interneurons, which were thought to be largely dependent on KCa channels.

6. the tertiary structure of the C-terminal domain of Kv1.3 is necessary and sufficient for Kv1.3- KCNE4 interaction.

7. promotes B lymphocyte activation, proliferation and monocyte chemotaxis

8. Changes in Kv1.3 subcellular distribution upon EGFR activation were due to Kv1.3 clathrin-dependent endocytosis, which targets the Kv1.3 channels to the lysosomal degradative pathway.

9. Kv1.3 channel serves as a negative regulator of phagocytosis in macrophages and can be a potential target in the treatment of macrophage dysfunction

10. concluded that Kv1.3 may stimulate macrophage migration through the activation of ERK.

11. A compensatory upregulation of the potassium channels K2P3.1 and KV1.3 seems to counterbalance the deletion of K2P5.1.

12. JAK2 participates in the signalling, regulating the voltage-gated K(+) channel KCNA3.

13. Antigenic Stimulation of Kv1.3-Deficient Th Cells Gives Rise to a Population of Foxp3-Independent T Cells with Suppressive Properties

14. A potent and selective peptide blocker of the Kv1.3 channel: prediction from free-energy simulations and experimental confirmation

15. Our studies suggest thatKv1.3 plays a unique role in neuronal differentiation and/or survival of interneuron populations of the cerebral cortex

16. Inhibition of NMDAR antagonists on the conductivity of Kv1.3 and KCa3.1 potassium channels was found.

17. A significant increase of Kv1.3 protein levels was observed after LPS challenge, an effect that was blunted by e-LXA4. Kv1.3 is required for the attenuation of NF-kappaB activity.

18. Results indicate the potential use of Kv1.3 blockers for the treatment of obesity and insulin resistance.

19. Exert inhibitory effects on thymocyte Kv1.3-channel currents.

20. Data indicate that ShK-K amide retained a high affinity for the voltage-gated potassium channel Kv1.3 channels (IC50 26 +/- 3 pM).