Cooperative endocytosis of the endosomal SNARE protein syntaxin-8 and the potassium channel TASK-1

Renigunta, Vijay; Fischer, Thomas; Zuzarte, Marylou; Kling, Stefan; Zou, Xinle; Siebert, K.; Limberg, Maren M.; Rinné, Susanne; Decher, Niels; Schlichthörl, Günter; Daut, Jürgen

doi:10.1091/mbc.e13-10-0592

Cited by 27 publications

(28 citation statements)

References 69 publications

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“…Human atrial cells lack a classic T-tubular system and accordingly the TASK-3 immunostaining does not give the typical cross striation pattern, as described for TASK-1 in rat ventricular cardiomyocytes [6]. TASK-1 channels were also detected in intracellular compartments, which is in accordance with the previously described retention and/or endocytosis of these channels [26,27]. In contrast, TASK-3 seems to be primarily localized at the plasma membrane ( Fig.…”

Section: Task-3 Expression In the Human Heartsupporting

confidence: 86%

TASK-1 and TASK-3 may form heterodimers in human atrial cardiomyocytes

Rinné

Kiper

Schlichthörl

et al. 2015

Journal of Molecular and Cellular Cardiology

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Section: Task-3 Expression In the Human Heartsupporting

confidence: 86%

TASK-1 and TASK-3 may form heterodimers in human atrial cardiomyocytes

Rinné

Kiper

Schlichthörl

et al. 2015

Journal of Molecular and Cellular Cardiology

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“…38 In addition, the patients' rhythm status was not associated with atrial resting membrane potential changes in the present study consistent with earlier work. 35,38,39 Similarly, inhibition of K 2P 3.1 current had no effect on resting membrane potential. The molecular basis of electric remodeling was further elucidated in a comprehensive approach that included all K 2P channels and 21 additional ion channel subunits relevant to atrial electrophysiology.…”

Section: Apd Shortening In Caf Patients: Significance Of K 2p 31 Andmentioning

confidence: 91%

“…There was no significant correlation between LV function and cardiac rhythm (F=11.8; P=0. 35 In the present work, we delineated mRNA expression of multiple K 2P channels in left and right atria obtained from control subjects with SR. K 2P 3.1 displayed highest transcript levels among K 2P family members with confirmed K + channel function (ie, after exclusion of K 2P 1.1, K 2P 7.1, K 2P 12.1, and K 2P 15.1 subunits, which do not produce substantial K + currents) and was specifically studied. The high ratio of atrial to ventricular K 2P 3.1 transcripts (16:1) highlighted predominantly atrial expression.…”

Section: Independent Effects Of Cardiac Function On Atrial K 2p 31 Ementioning

confidence: 99%

Upregulation of K _2P 3.1 K ⁺ Current Causes Action Potential Shortening in Patients With Chronic Atrial Fibrillation

et al. 2015

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Background-Antiarrhythmic management of atrial fibrillation (AF) remains a major clinical challenge. Mechanismbased approaches to AF therapy are sought to increase effectiveness and to provide individualized patient care. K 2P 3.1 (TASK-1 [tandem of P domains in a weak inward-rectifying K + channel-related acid-sensitive K + channel-1]) 2-poredomain K + (K 2P ) channels have been implicated in action potential regulation in animal models. However, their role in the pathophysiology and treatment of paroxysmal and chronic patients with AF is unknown. Methods and Results-Right and left atrial tissue was obtained from patients with paroxysmal or chronic AF and from control subjects in sinus rhythm. Ion channel expression was analyzed by quantitative real-time polymerase chain reaction and Western blot. Membrane currents and action potentials were recorded using voltage-and current-clamp techniques. K 2P 3.1 subunits exhibited predominantly atrial expression, and atrial K 2P 3.1 transcript levels were highest among functional K 2P channels. K 2P 3.1 mRNA and protein levels were increased in chronic AF. Enhancement of corresponding currents in the right atrium resulted in shortened action potential duration at 90% of repolarization (APD 90 ) compared with patients in sinus rhythm. In contrast, K 2P 3.1 expression was not significantly affected in subjects with paroxysmal AF. Pharmacological K 2P 3.1 inhibition prolonged APD 90 in atrial myocytes from patients with chronic AF to values observed among control subjects in sinus rhythm. Conclusions-Enhancement of atrium-selective K 2P 3.1 currents contributes to APD shortening in patients with chronic AF, and K 2P 3.1 channel inhibition reverses AF-related APD shortening. These results highlight the potential of K 2P 3.1 as a novel drug target for mechanism-based AF therapy.

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“…It seems quite possible that the level of expression and the hypoxic sensitivity of TASK may be modified in chronic hypoxia to produce such changes in cellular and physiological responses. Cell surface expression of TASK is regulated by a number of cellular signals [51,67], and it seems likely that chronic hypoxia can modify the function of these signals to alter the expression level. Chronic hypoxia can also alter mitochondrial function to sensitize TASK to hypoxia.…”

Section: Task1/3 As the Hypoxia-sensitive Background K+ Channel In Camentioning

confidence: 99%

Role of K2P channels in stimulus-secretion coupling

Kim

Kang

2014

Pflugers Arch - Eur J Physiol

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Two-pore domain K+ (K2P) channels are involved in a variety of physiological processes by virtue of their high basal activity and sensitivity to various biological stimuli. One of these processes is secretion of hormones and transmitters in response to stimuli such as hypoxia, acidosis and receptor agonists. The rise in intracellular [Ca2+] ([Ca2+]i) that is critical for the secretory event can be achieved by several mechanisms: (a) Inhibition of resting (background) K+ channels, (b) activation of Na+/Ca2+-permeable channels and (c) release of Ca2+ from intracellular stores. Here, we discuss the role of TASK and TREK in stimulus-secretion mechanisms in carotid body chemoreceptor cells and adrenal medullary/cortical cells. Studies show that stimuli such as hypoxia and acidosis cause cell depolarization and transmitter/hormone secretion by inhibition of TASK or TREK. Subsequent elevation of [Ca2+]i produced by opening of voltage-dependent Ca2+ channels then activates a Na+-permeable cation channel, presumably to help sustain the depolarization and [Ca2+]i. Agonists such as angiotensin II may elevate [Ca2+]i via multiple mechanisms involving both inhibition of TASK/TREK and Ca2+ release from internal stores to cause aldosterone secretion. Thus, inhibition of resting (background) K+ channels and subsequent activation of voltage-gated Ca2+ channels and Na+-permeable non-selective cation channels may be a common ionic mechanism that lead to hormone and transmitter secretion.

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Cooperative endocytosis of the endosomal SNARE protein syntaxin-8 and the potassium channel TASK-1

Cited by 27 publications

References 69 publications

TASK-1 and TASK-3 may form heterodimers in human atrial cardiomyocytes

TASK-1 and TASK-3 may form heterodimers in human atrial cardiomyocytes

Upregulation of K _2P 3.1 K ⁺ Current Causes Action Potential Shortening in Patients With Chronic Atrial Fibrillation

Role of K2P channels in stimulus-secretion coupling

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Cooperative endocytosis of the endosomal SNARE protein syntaxin-8 and the potassium channel TASK-1

Cited by 27 publications

References 69 publications

TASK-1 and TASK-3 may form heterodimers in human atrial cardiomyocytes

TASK-1 and TASK-3 may form heterodimers in human atrial cardiomyocytes

Upregulation of K 2P 3.1 K + Current Causes Action Potential Shortening in Patients With Chronic Atrial Fibrillation

Role of K2P channels in stimulus-secretion coupling

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Upregulation of K _2P 3.1 K ⁺ Current Causes Action Potential Shortening in Patients With Chronic Atrial Fibrillation