Tyrosine Phosphorylation-dependent Suppression of a Voltage-gated K+ Channel in T Lymphocytes upon Fas Stimulation

Szabó, Ildikò; Gulbins, Erich; Apfel, H.; Zhang, Xinfeng; Barth, Petra; Büsch, Andreas; Schlottmann, Klaus; Pongs, Olaf; Läng, Florian

doi:10.1074/jbc.271.34.20465

Cited by 208 publications

(178 citation statements)

References 26 publications

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“…(Soliven et al, 1991;Dubois and Rouzaire-Dubois, 1993;Bright et al, 1994;Duprat et al, 1995;Szabo et al, 1996;Wang et al, 1999a,b;Lu et al, 2003;Gao et al, 2004;Guo et al, 2005). For example, we, as well as other researchers, have shown that stimulation of K + channel activity and dramatic loss of intracellular K + can result in apoptosis in the corneal epithelium, neurons, myeloblastic ML-1 cells, and other cell types (Schulz et al, 1996;Eldadah et al, 1997;Yu et al, 1997;Wang et al, 1999aWang et al, ,2003Lu et al, 2003;Trimarchi et al, 2002;Remillard and Yuan, 2004).…”

Section: Introductionmentioning

confidence: 68%

“…Various investigations have shown that K + channel activity can be affected by apoptosis inducers, including ROS, Fas ligand and TNF, and anticancer drugs (Soliven et al, 1991;Dubois and Rouzaire-Dubois, 1993;Bright et al, 1994;Duprat et al, 1995;Szabo et al, 1996). There is growing evidence showing that K + channel activities are probably involved in programmed cell death in many cell types (Schulz et al, 1996;Eldadah et al, 1997;Yu et al, 1997;Wang et al, 1999b).…”

Section: Kv Channel Mediating Uv-induced Apoptosismentioning

confidence: 99%

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Stress-induced corneal epithelial apoptosis mediated by K+ channel activation

2006

Progress in Retinal and Eye Research

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One of the functional roles of the corneal epithelial layer is to protect the cornea, lens and other underlying ocular structures from damages caused by environmental insults. It is important for corneal epithelial cells to maintain this function by undergoing continuous renewal through a dynamic process of wound healing. Previous studies in corneal epithelial cells have provided substantial evidence showing that environmental insults, such as ultraviolet (UV) irradiation and other biohazards, can induce stress-related cellular responses resulting in apoptosis and thus interrupt the dynamic process of wound healing. We found that UV irradiation-induced apoptotic effects in corneal epithelial cells are started by the hyperactivation of K + channels in the cell membrane resulting in a fast loss of intracellular K + ions. Recent studies provide further evidence indicating that these complex responses in corneal epithelial cells are resulted from the activation of stressrelated signaling pathways mediated by K + channel activity. The effect of UV irradiation on corneal epithelial cell fate shares common signaling mechanisms involving the activation of intracellular responses that are often activated by the stimulation of various cytokines. One piece of evidence for making this distinction is that at early times UV irradiation activates a Kv3.4 channel in corneal epithelial cells to elicit activation of c-Jun N-terminal kinase cascades and p53 activation leading to cell cycle arrest and apoptosis. The hypothetic model is that UV-induced potassium channel hyperactivity as an early event initiates fast cell shrinkages due to the loss of intracellular potassium, resulting in the activation of scaffolding protein kinases and cytoskeleton reorganizations. This review article presents important control mechanisms that determine Kv channel activity-mediated cellular responses in corneal epithelial cells, involving activation of stress-induced signaling pathways, arrests of cell cycle progression and/or induction of apoptosis.

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Section: Introductionmentioning

confidence: 68%

Section: Kv Channel Mediating Uv-induced Apoptosismentioning

confidence: 99%

Stress-induced corneal epithelial apoptosis mediated by K+ channel activation

2006

Progress in Retinal and Eye Research

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Section: Ceramidementioning

confidence: 99%

“…Further, ceramide has been shown to regulate the activity of the potassium channel Kv1.3 and calcium release-activated calcium (CRAC) channels [59-60]. Ceramide inhibits the activity of these ion channels in the cell membrane [59-62]. At present it is unknown how ceramide affects the activity of ion channels, but it might be possible that ceramide alters ion channels by a direct interference or by the change of the lipid composition in the environment of the channel [62].…”

Section: Ceramidementioning

confidence: 99%

The Role of Sphingolipids and Ceramide in Pulmonary Inflammation in Cystic Fibrosis

Becker

Riethmüller²,

Zhang³

et al. 2010

TORMJ

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Sphingolipids and in particular ceramide have been shown to be critically involved in the response to many receptor-mediated, but also receptor-independent, mainly stress stimuli. Recent studies demonstrate that ceramide plays an important role in the pathogenesis of cystic fibrosis, a hereditary metabolic disorder caused by mutations of the Cystic Fibrosis Transmembrane Conductance Regulator. Patients with cystic fibrosis suffer from chronic pulmonary inflammation and microbial lung infections, in particular with Pseudomonas aeruginosa. Chronic pulmonary inflammation in these patients seems to be the initial pathophysiological event. Inflammation may finally result in the high infection susceptibility of these patients, fibrosis and loss of lung function. Recent studies demonstrated that ceramide accumulates in lungs of cystic fibrosis mice and causes age-dependent pulmonary inflammation as indicated by accumulation of neutrophils and macrophages in the lung and increased pulmonary concentrations of Interleukins 1 and 8, death of bronchial epithelial cells, deposition of DNA in bronchi and high susceptibility to Pseudomonas aeruginosa infections. Genetic or pharmacological inhibition of the acid sphingomyelinase blocks excessive ceramide production in lungs of cystic fibrosis mice and corrects pathological lung findings. First clinical studies confirm that inhibition of the acid sphingomyelinase with small molecules might be a novel strategy to treat patients with cystic fibrosis.

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“…Perturbations in potassium levels in neurons and decreased potassium levels in T cells directly cause apoptosis. [147][148][149] Interestingly, both Bcl-2 and Bax also have ion channel properties and may enhance ion-channel formation. [150][151][152] Vpu has a large effect on the susceptibility of cells to Fasinduced apoptosis.…”

Section: Vpumentioning

confidence: 99%