Up-regulation of the IKCa1 Potassium Channel during T-cell Activation

Ghanshani, Sanjiv; Wulff, Heike; Miller, Mark J.; Rohm, H.; Neben, Amber L.; Gutman, George A.; Cahalan, Michael D.; Chandy, K. George

doi:10.1074/jbc.m003941200

Cited by 367 publications

(453 citation statements)

References 51 publications

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“…The SK3 protein is abundant in porcine coronary endothelial cells, and immunofluorescent labelling confirms that IK1 and SK3 are expressed at the plasmalemma of porcine coronary endothelial cells [21]. In addition, it is well documented that in a number of cell types such as lymphocytes [22] and fibroblasts [23,24], IK1 expression is highly variable during the different phases of cell proliferation. By contrast, in human colonic and cavernosal vascular endothelium, no IK1 immunoreactivity was detected [20].…”

Section: Discussionmentioning

confidence: 59%

Reduced expression of SK3 and IK1 channel proteins in the cavernous tissue of diabetic rats

Jun¹,

Jia²,

Xu³

et al. 2010

Asian J Androl

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The small (SK3) and intermediate (IK1) conductance calcium-activated potassium channels could have key roles in the endothelium-dependent hyperpolarization factor pathway, which is believed to contribute to normal penile erection function. We aimed to investigate the expression of SK3 and IK1 in diabetic rodents. The experimental diabetes model was induced in 8-week-old male Sprague-Dawley rats (250-300 g) by a single administration of streptozotocin. Both the diabetes mellitus group (DM group, n = 20) and the control group (NDM group, n = 10) were injected with a low dose of apomorphine to allow for the measurement and comparison of the corresponding penile erections. The mRNA and protein expression levels of SK3 and IK1 were measured by reverse transcription polymerase chain reaction and western blot, respectively. Erectile function was significantly decreased in the DM group compared with control group (P < 0.05). The mRNA and protein expression levels of SK3 and IK1 were reduced in the cavernous tissue of diabetic rats compared with the control group (P < 0.05). Diabetes inhibits mRNA and protein expression of both SK3 and IK1 in the cavernous tissue of diabetic rats. This could play a key role in the development of erectile dysfunction in diabetic rats.

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Section: Discussionmentioning

confidence: 59%

Reduced expression of SK3 and IK1 channel proteins in the cavernous tissue of diabetic rats

Jun¹,

Jia²,

Xu³

et al. 2010

Asian J Androl

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show abstract

“…Our findings that clotrimazole or TRAM-34 blocked the IKCa1 current and cell proliferation in HEC-1-A cells are consistent with this explanation. It has been known that cells in the early G 1 phase are depolarized; however, they are hyperpolarized during the progression through G 1 into the S phase (Wang et al, 1998;Ghanshani et al, 2000). Inhibition of K þ channels leads to membrane depolarization and cellcycle arrest in early G 1 phase in the MCF-7 human breast carcinoma cell line (Wang et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Blockage of intermediate-conductance-Ca2+-activated K+ channels inhibits progression of human endometrial cancer

et al. 2007

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“…This is supported by previous reports, in which ERK induces an increase of proliferative gene expression, eg, the AP-1 family member c-fos, [25][26][27] and the increased production of c-fos leads to induction of K Ca 3.1 expression through AP-1 promoter elements. 28 In addition to the upregulation of K Ca 3.1 current and K Ca 3.1 expression by AGEs, the recent studies reported that K Ca 3.1 channels were activated by PI(3)P, which is produced by PI3K from phosphatidylinositol. [29][30][31] Decreasing intracellular level of PI(3)P can reduce K Ca 3.1 channel activity.…”

Section: Discussionmentioning

confidence: 99%

KCa3.1 channels mediate the increase of cell migration and proliferation by advanced glycation endproducts in cultured rat vascular smooth muscle cells

Zhao

Wang

et al. 2013

Laboratory Investigation

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The mechanisms underlying the involvement of advanced glycation endproducts (AGEs) in diabetic atherosclerosis are not fully understood. The present study was designed to investigate whether intermediate-conductance Ca 2 þ -activated K þ channels (K Ca 3.1 channels) are involved in migration and proliferation induced by AGEs in cultured rat vascular smooth muscle cells (VSMCs) using approaches of whole-cell patch voltage-clamp, cell proliferation and migration assay, and western blot analysis. It was found that the current density and protein level of K Ca 3.1 channels were enhanced in cells incubated with AGE-BSA (bovine serum albumin), and the effects were reversed by co-incubation of AGE-BSA with anti-RAGE (anti-receptors of AGEs) antibody. The ERK1/2 inhibitors PD98059 and U0126, the P38-MAPK inhibitors SB203580 and SB202190, or the PI3K inhibitors LY294002 and wortmannin countered the K Ca 3.1 channel expression by AGE-BSA. In addition, AGE-BAS increased cell migration and proliferation, and the effects were fully reversed with anti-RAGE antibody, the K Ca 3.1 channel blocker TRAM-34, or K Ca 3.1 small interfering RNA. These results demonstrate for the first time that AGEs-induced increase of migration and proliferation is related to the upregulation of K Ca 3.1 channels in rat VMSCs, and the intracellular signals ERK1/2, P38-MAPK and PI3K are involved in the regulation of K Ca 3.1 channel expression.

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Up-regulation of the IKCa1 Potassium Channel during T-cell Activation

Cited by 367 publications

References 51 publications

Reduced expression of SK3 and IK1 channel proteins in the cavernous tissue of diabetic rats

Reduced expression of SK3 and IK1 channel proteins in the cavernous tissue of diabetic rats

Blockage of intermediate-conductance-Ca2+-activated K+ channels inhibits progression of human endometrial cancer

KCa3.1 channels mediate the increase of cell migration and proliferation by advanced glycation endproducts in cultured rat vascular smooth muscle cells

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