Recombinant Mouse Intermediate conductance calcium-activated potassium channel protein 4 (Kcnn4)

1. KCa3.1 channel is likely to be a critical target on the oxidative stress. PMID:28455747
2. Diet-induced hyperhomocysteinemia enhanced myoendothelial feedback, and increased Cx37 and IK1 expression may contribute. nNOS or iNOS did not upregulate to compensate for decreased eNOS, and they had little involvement in vasomotor function. PMID:28857417
3. The Intermediate-conductance calmodulin/calcium-activated K+ channels 3.1 (KCa3.1-/- knockout mice) significantly reduced corneal fibrosis and expression of pro-fibrotic marker genes, suggesting that KCa3.1 plays an important role corneal wound healing in vivo. PMID:29554088
4. KCa3.1(-/-) mice exhibited significantly smaller infarct areas in a model of ischemic stroke. PMID:29037241
5. KCa3.1(-/-) mice demonstrated normal behavioral responses in models of acute nociceptive, persistent inflammatory, and persistent neuropathic pain. However, their behavioral responses to noxious chemical stimuli such as formalin and capsaicin were increased. Accordingly, formalin-induced nociceptive behavior was increased in wild-type mice after administration of the KCa3.1 inhibitor TRAM-34. PMID:28823609
6. SK4 activity is crucial for cell cycle control. PMID:28557306
7. Deletion of KCa3.1 reduced astrogliosis and rescued memory loss induced by intrahippocampal Abeta1-42 peptide injection. PMID:27567685
8. Blocking KCa3.1 suppresses plaque instability in advanced stages of atherosclerosis by inhibiting macrophage polarization toward an M1 phenotype. PMID:28062499
9. enhanced KCa 3.1 activity may compensate for decreased nitric oxide signaling during vascular aging. PMID:27363720
10. Findings highlight a novel role for intermediate-conductance calcium-activated potassium channel (KCa3.1) in phenotypic modulation of reactive astrocytes and in astrocyte mobilization in response to mechanical stress, providing a potential target for therapeutic intervention in brain injuries. PMID:27163196
11. alpha1D Ca and SK4 channels are coupled in the atria, and deletion of alpha1D leads to decreased SK4 mRNA and BNP secretion providing evidence for a novel role of alpha1D in atrial endocrine function PMID:27884747
12. KCa3.1 blockade protects against cisplatin-induced acute kidney injury through the attenuation of apoptosis by interference with intrinsic apoptotic and endoplasmic reticulum stress-related mediators. PMID:26438401
13. The results suggest that KCa3.1 activation contributes to dysfunctional tubular autophagy in diabetic nephropathy through PI3K/Akt/mTOR signaling pathways. PMID:27029904
14. These results indicate that IK1 channels do not mediate the a slow afterhyperpolarization in pyramidal neurons. PMID:26765773
15. KCa3.1 is a possible marker of M/MPhi in the protumor state and a potential therapeutic target to induce glioma-associated microglia/macrophages to re-acquire a pro-inflammatory, antitumor activity. PMID:27054329
16. that KCa3.1 channels are key actors in the migration capacity of neutrophils, and its inhibition did not affect other relevant cellular functions PMID:26138196
17. Modulation of PKA and PI3KC2beta activity to control of KCa3.1 channel expression can be an alternative important target to attenuate ascending thoracic aortic aneurysms in Fabry disease. PMID:26820527
18. These findings suggest that the KCa3.1 channel can serve as a new target to attenuate and prevent development of ascending thoracic aortic aneurysm in Fabry disease. PMID:26592662
19. Inhibition of K(Ca)3.1 by EETs (14,15-EET), 20-HETE, and omega3 critically depended on the presence of electron double bonds and hydrophobicity within the 10 carbons preceding the carboxyl-head of the molecules. PMID:25372486
20. NDPKB/SK4 signaling is required for neointima formation in injured carotid arteries. PMID:26088577
21. KCa 3.1 blockade strongly reduced the growth of xenografted NSCLC cells. PMID:25704182
22. The data suggest that the P2Y2/4 receptor activation elicits blood pressure responses via distinct mechanisms involving KCa3.1 and Cx37. PMID:25545736
23. Overexpression of CCL20 in human proximal tubular cells is inhibited by blockade of KCa3.1 under diabetic conditions through inhibition of the NF-kappaB pathway. PMID:24733189
24. Studies suggest an important modulatory role for KCa3.1 in adult neuroblast migration that could be capitalized on in future attempts to alter the intrinsic repair response of the brain using neuronal precursor cells PMID:23585521
25. Role of the K(Ca)3.1 K+ channel in auricular lymph node CD4+ T-lymphocyte function of the delayed-type hypersensitivity model PMID:23594188
26. Pulmonary hypertension in wild type mice and animals with genetic deficit in KCa2.3 and KCa3.1 channels PMID:24858807
27. blockade of KCa3.1 attenuates diabetic renal interstitial fibrogenesis through inhibiting activation of fibroblasts PMID:24166472
28. Targeted inhibition of KCa3.1 reduces reactive gliosis in cultured astrocytes. PMID:24606313
29. increase in KCa3.1 activity induced by the upregulation of KCa3.1a and NDPK-B may be involved in the pathogenesis of IBD by mediating the enhancement of the proliferative response in MLN CD4(+) T lymphocyte. PMID:24674776
30. Globotriaosylceramide accelerates the endocytosis and lysosomal degradation of endothelial KCa3.1 via a clathrin-dependent process, leading to endothelial dysfunction in Fabry disease. PMID:24158513
31. IK1, and to some extent SK3, channels exert a substantial positive feedback influence on endothelial Ca(2+) dynamics in agonist stimulated mesenteric arteries. PMID:24177326
32. Blockade of KCa3.1 with potassium channel blockers prevented airway remodeling in allergic asthma. PMID:23492185
33. The inhibition of KCa3.1 channels activity reduces cell motility in glioblastoma derived cancer stem cells. PMID:23110108
34. Genetic KCa3.1-deficiency causes locomotor hyperactivity and altered monoamine levels in selected brain regions PMID:23077667
35. KCa3.1 channels are involved in the pathogenesis of obliterative airway disease (OAD). KCa3.1 blockade holds promise to reduce OAD development. PMID:23325003
36. Modafinil inhibits K(Ca)3.1 channels and vascular smooth muscle contraction by cAMP-dependent phosphorylation. PMID:22414869
37. KCa3.1 expression in lung dendritic cells was up-regulated by ovalbumin sensitization. KCa3.1 was involved in the migration of lung dendritic cells to lymphatic chemokines. PMID:21493782
38. Ca2+ activated K+ channel Kca3.1 plays a central role in gastric acid secretion. PMID:21691077
39. the N-terminal domain of K(Ca)3.1 is critical for channel trafficking to the plasma membrane PMID:21345794
40. Globotriaosylceramide evokes K(Ca)3.1 channel dysfunction, and the channel dysfunction in vascular endothelial cells may contribute to vasculopathy in Fabry disease. PMID:20971723
41. The SK4 component of the Kslow current can trigger oscillations in mice without functioning KATP channels. PMID:21099262
42. Kcnn4 is crucially involved in cardiac and cardiac pacemaker cell differentiation of embryonic stem cells PMID:20956206
43. K(Ca)3.1 channel activity and Gardos effect counteract hemolysis of injured erythrocytes, thus decreasing hemoglobin release into circulating blood. PMID:20857305
44. Nucleoside diphosphate kinase B knock-out mice have impaired activation of the K+ channel KCa3.1, resulting in defective T cell activation PMID:20884616
45. found that inhibition of KCa3.1(-/-) protected mice from developing severe colitis in mouse models of inflammatory bowel disease. PMID:20080610
46. Selective blockade of T-lymphocyte K(Ca)3.1 and K(v)1.3 channels may represent a novel alternative therapy for prevention of kidney allograft rejection. PMID:19715983
47. SK1, -2, -3, and IK1 (SK4) are expressed in islet cells and insulin-secreting cells and are able to influence glucose-induced calcium responses, thereby regulating insulin secretion. PMID:12882916
48. Results confirm that IK channels in red blood cells, T lymphocytes, and parotid acinar cells are indeed encoded by the Kcnn4 gene. PMID:15347667
49. cardiac Ang II overproduction leads to the emergence of a long QT syndrome resulting from an IK1-dependent prolongation of the action potential duration through modulation of channel subunit expression. PMID:17070838
50. Submandibular acinar cell function relies on KCNN4 channel activity. PMID:17379640

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UNIGENE: Mm.9911

KEGG: mmu:16534

STRING: 10090.ENSMUSP00000133065