Relevant bibliographies by topics / HTREK-1

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Academic literature on the topic 'HTREK-1'

Author: Grafiati
Published: 6 September 2023

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Journal articles on the topic "HTREK-1"

1

Wiedmann, Felix, Daniel Schlund, Francisco Faustino, Manuel Kraft, Antonius Ratte, Dierk Thomas, Hugo A. Katus, and Constanze Schmidt. "N-Glycosylation of TREK-1/hK2P2.1 Two-Pore-Domain Potassium (K2P) Channels." International Journal of Molecular Sciences 20, no. 20 (October 20, 2019): 5193. http://dx.doi.org/10.3390/ijms20205193.

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Mechanosensitive hTREK-1 two-pore-domain potassium (hK2P2.1) channels give rise to background currents that control cellular excitability. Recently, TREK-1 currents have been linked to the regulation of cardiac rhythm as well as to hypertrophy and fibrosis. Even though the pharmacological and biophysical characteristics of hTREK-1 channels have been widely studied, relatively little is known about their posttranslational modifications. This study aimed to evaluate whether hTREK-1 channels are N-glycosylated and whether glycosylation may affect channel functionality. Following pharmacological inhibition of N-glycosylation, enzymatic digestion or mutagenesis, immunoblots of Xenopus laevis oocytes and HEK-293T cell lysates were used to assess electrophoretic mobility. Two-electrode voltage clamp measurements were employed to study channel function. TREK-1 channel subunits undergo N-glycosylation at asparagine residues 110 and 134. The presence of sugar moieties at these two sites increases channel function. Detection of glycosylation-deficient mutant channels in surface fractions and recordings of macroscopic potassium currents mediated by these subunits demonstrated that nonglycosylated hTREK-1 channel subunits are able to reach the cell surface in general but with seemingly reduced efficiency compared to glycosylated subunits. These findings extend our understanding of the regulation of hTREK-1 currents by posttranslational modifications and provide novel insights into how altered ion channel glycosylation may promote arrhythmogenesis.
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2

Dallas, Mark L., Jason L. Scragg, and Chris Peers. "Modulation of hTREK-1 by carbon monoxide." NeuroReport 19, no. 3 (February 2008): 345–48. http://dx.doi.org/10.1097/wnr.0b013e3282f51045.

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3

Woo, JooHan, Young Keul Jeon, Yin-Hua Zhang, Joo Hyun Nam, Dong Hoon Shin, and Sung Joon Kim. "Triple arginine residues in the proximal C-terminus of TREK K+ channels are critical for biphasic regulation by phosphatidylinositol 4,5-bisphosphate." American Journal of Physiology-Cell Physiology 316, no. 3 (March 1, 2019): C312—C324. http://dx.doi.org/10.1152/ajpcell.00417.2018.

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TWIK-related two-pore domain K+ channels (TREKs) are activated by acidic intracellular pH (pHi), membrane stretch, temperature, and arachidonic acid (AA). Phosphatidylinositol 4,5-bisphosphate (PIP2) exerts concentration-dependent biphasic regulations, which have been observed: inhibition by high PIP2, activation by partial decrease of PIP2, and inhibition by depletion of PIP2. Consistently, the stimulation of voltage-sensitive PIP2 phosphatase (Dr-VSP) induces initial activation and subsequent inhibition of TREKs. Lys in the proximal C-terminus (pCt) is responsible for the inhibition by high PIP2, which is generated by phosphatidylinositol kinases with ATP; its neutralizing mutation [K330A of human TREK-2 (hTREK-2)] induces tonic high activity, irrespective of ATP. Here we focus on triple successive Arg in pCt (R3-pCt) as a candidate region for the stimulatory regulation by lower PIP2. Their neutralized mutant (R3A-pCt; RRR340-2A and RRR355-7A in hTREK-1 and -2, respectively) showed negligible basal current and was not affected by ATP removal or by Dr-VSP activation. Phosphatidic acid, a phospholipid agonist of TREKs, did not activate R3A-pCt. In contrast, acidic pHi, AA, and high temperature activated R3A-pCt normally, whereas activation by membrane stretch was attenuated. In hTREK-2, combined neutralizations of the inhibitory K330 and R3-pCt (K330A/RRR355-7A) did not recover the suppressed current. In contrast, combined neutralization of pHi-sensing Glu (E332A/R355-7A) induced tonic high current and no further activation by pHi. Interestingly, when the Gly between K330/E332 and R3-pCt was mutated (G334A), hTREK-2 was tonic activated with reversed responses to ATP and acidic pHi. Therefore, we propose that the PIP2-dependent converse regulation of TREKs by Lys and R3-pCt with Gly implies structural flexibility.
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4

Mukherjee, Sourajit, and Sujit Sikdar. "Polymodal sensitivity of hTREK-1 channel to ischemia related factors." IBRO Reports 6 (September 2019): S361. http://dx.doi.org/10.1016/j.ibror.2019.07.1147.

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5

Miller, P., P. J. Kemp, A. Lewis, C. G. Chapman, H. J. Meadows, and C. Peers. "Acute hypoxia occludes hTREK-1 modulation: re-evaluation of the potential role of tandem P domain K+ channels in central neuroprotection." Journal of Physiology 548, no. 1 (February 28, 2003): 31–37. http://dx.doi.org/10.1113/jphysiol.2003.040048.

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6

Enyeart, John J., and Judith A. Enyeart. "Ca2+ and K+ channels of normal human adrenal zona fasciculata cells: Properties and modulation by ACTH and AngII." Journal of General Physiology 142, no. 2 (July 15, 2013): 137–55. http://dx.doi.org/10.1085/jgp.201310964.

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In whole cell patch clamp recordings, we found that normal human adrenal zona fasciculata (AZF) cells express voltage-gated, rapidly inactivating Ca2+ and K+ currents and a noninactivating, leak-type K+ current. Characterization of these currents with respect to voltage-dependent gating and kinetic properties, pharmacology, and modulation by the peptide hormones adrenocorticotropic hormone (ACTH) and AngII, in conjunction with Northern blot analysis, identified these channels as Cav3.2 (encoded by CACNA1H), Kv1.4 (KCNA4), and TREK-1 (KCNK2). In particular, the low voltage–activated, rapidly inactivating and slowly deactivating Ca2+ current (Cav3.2) was potently blocked by Ni2+ with an IC50 of 3 µM. The voltage-gated, rapidly inactivating K+ current (Kv1.4) was robustly expressed in nearly every cell, with a current density of 95.0 ± 7.2 pA/pF (n = 64). The noninactivating, outwardly rectifying K+ current (TREK-1) grew to a stable maximum over a period of minutes when recording at a holding potential of −80 mV. This noninactivating K+ current was markedly activated by cinnamyl 1-3,4-dihydroxy-α-cyanocinnamate (CDC) and arachidonic acid (AA) and inhibited almost completely by forskolin, properties which are specific to TREK-1 among the K2P family of K+ channels. The activation of TREK-1 by AA and inhibition by forskolin were closely linked to membrane hyperpolarization and depolarization, respectively. ACTH and AngII selectively inhibited the noninactivating K+ current in human AZF cells at concentrations that stimulated cortisol secretion. Accordingly, mibefradil and CDC at concentrations that, respectively, blocked Cav3.2 and activated TREK-1, each inhibited both ACTH- and AngII-stimulated cortisol secretion. These results characterize the major Ca2+ and K+ channels expressed by normal human AZF cells and identify TREK-1 as the primary leak-type channel involved in establishing the membrane potential. These findings also suggest a model for cortisol secretion in human AZF cells wherein ACTH and AngII receptor activation is coupled to membrane depolarization and the activation of Cav3.2 channels through inhibition of hTREK-1.
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El Hachmane, Mickael-F., Kathryn A. Rees, Emma L. Veale, Vadim V. Sumbayev, and Alistair Mathie. "Enhancement of TWIK-related Acid-sensitive Potassium Channel 3 (TASK3) Two-pore Domain Potassium Channel Activity by Tumor Necrosis Factor α." Journal of Biological Chemistry 289, no. 3 (December 4, 2013): 1388–401. http://dx.doi.org/10.1074/jbc.m113.500033.

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TASK3 two-pore domain potassium (K2P) channels are responsible for native leak K channels in many cell types which regulate cell resting membrane potential and excitability. In addition, TASK3 channels contribute to the regulation of cellular potassium homeostasis. Because TASK3 channels are important for cell viability, having putative roles in both neuronal apoptosis and oncogenesis, we sought to determine their behavior under inflammatory conditions by investigating the effect of TNFα on TASK3 channel current. TASK3 channels were expressed in tsA-201 cells, and the current through them was measured using whole cell voltage clamp recordings. We show that THP-1 human myeloid leukemia monocytes, co-cultured with hTASK3-transfected tsA-201 cells, can be activated by the specific Toll-like receptor 7/8 activator, R848, to release TNFα that subsequently enhances hTASK3 current. Both hTASK3 and mTASK3 channel activity is increased by incubation with recombinant TNFα (10 ng/ml for 2–15 h), but other K2P channels (hTASK1, hTASK2, hTREK1, and hTRESK) are unaffected. This enhancement by TNFα is not due to alterations in levels of channel expression at the membrane but rather to an alteration in channel gating. The enhancement by TNFα can be blocked by extracellular acidification but persists for mutated TASK3 (H98A) channels that are no longer acid-sensitive even in an acidic extracellular environment. TNFα action on TASK3 channels is mediated through the intracellular C terminus of the channel. Furthermore, it occurs through the ASK1 pathway and is JNK- and p38-dependent. In combination, TNFα activation and TASK3 channel activity can promote cellular apoptosis.
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Chen, X. J., W. Zheng, L. L. Chen, Z. B. Chen, and S. Q. Wang. "Telomerase antisense inhibition for the proliferation of endometrial cancer in vitro and in vivo." International Journal of Gynecologic Cancer 16, no. 6 (2006): 1987–93. http://dx.doi.org/10.1111/j.1525-1438.2006.00734.x.

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The objective of this study was to investigate the antitumor effect of antisense telomerase oligodeoxynucleotides to endometrial cancer cells in vitro and in vivo. Antisense oligodeoxynucleotides (ODNs) against the human telomerase transcripatse (hTERT) synthesized to serve as telomerase inhibitors. Reverse transcription–polymerase chain reaction and 3-[4,5-dimethylthiazol-2yl]-2,5-diphenyltetrazolium bromide (MTT) assay were used to test the expression of hTERT messengerRNA (mRNA) and inhibition of cell proliferation in vitro. In vivo, antitumor effects of ODNs or combined with cisplatin were evaluated in endometrial cancer xenograft. Telomerase activity was tested by telomeric repeat amplification protocol. Antisense ODNs could inhibit proliferation of human endometrial cancer cells (HEC-1-A) in vitro, and downregulate the expression hTRET mRNA in a dose- and period-dependent manner. The tumor growth inhibitory rate of low- and high-dose ODNs were 34.20% and 89.21%, and combined group was 75.30%. Telomerase activity was downregulated to 87.32% compared to the control in the ODNs-treated xenograft tumors. Antisense oligonucleotides of hTERT effectively inhibit the growth of endometrial cancer cell line. Telomerase inhibitor might be a new strategy for chemotherapy or chemoprevention in endometrial cancer.
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9

Gil, V., D. Gallego, H. Moha Ou Maati, R. Peyronnet, M. Martínez-Cutillas, C. Heurteaux, M. Borsotto, and M. Jiménez. "Relative contribution of SKCa and TREK1 channels in purinergic and nitrergic neuromuscular transmission in the rat colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no. 3 (August 1, 2012): G412—G423. http://dx.doi.org/10.1152/ajpgi.00040.2012.

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Purinergic and nitrergic neurotransmission predominantly mediate inhibitory neuromuscular transmission in the rat colon. We studied the sensitivity of both purinergic and nitrergic pathways to spadin, a TWIK-related potassium channel 1 (TREK1) inhibitor, apamin, a small-conductance calcium-activated potassium channel blocker and 1H-[1,2,4]oxadiazolo[4,3-α]quinoxalin-1-one (ODQ), a specific inhibitor of soluble guanylate cyclase. TREK1 expression was detected by RT-PCR in the rat colon. Patch-clamp experiments were performed on cells expressing hTREK1 channels. Spadin (1 μM) reduced currents 1) in basal conditions 2) activated by stretch, and 3) with arachidonic acid (AA; 10 μM). l-Methionine (1 mM) or l-cysteine (1 mM) did not modify currents activated by AA. Microelectrode and muscle bath studies were performed on rat colon samples. l-Methionine (2 mM), apamin (1 μM), ODQ (10 μM), and Nω-nitro-l-arginine (l-NNA; 1 mM) depolarized smooth muscle cells and increased motility. These effects were not observed with spadin (1 μM). Purinergic and nitrergic inhibitory junction potentials (IJP) were studied by incubating the tissue with l-NNA (1 mM) or MRS2500 (1 μM). Both purinergic and nitrergic IJP were unaffected by spadin. Apamin reduced both IJP with a different potency and maximal effect for each. ODQ concentration dependently abolished nitrergic IJP without affecting purinergic IJP. Similar effects were observed in hyperpolarizations induced by sodium nitroprusside (1 μM) and nitrergic relaxations induced by electrical stimulation. We propose a pharmacological approach to characterize the pathways and function of purinergic and nitrergic neurotransmission. Nitrergic neurotransmission, which is mediated by cyclic guanosine monophosphate, is insensitive to spadin, an effective TREK1 channel inhibitor. Both purinergic and nitrergic neurotransmission are inhibited by apamin but with different relative sensitivity.
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10

Lee, Seungho, Guen Young Lee, Sujin Kim, Yong-Beom Park, and Han-Jun Lee. "Clinical utility of fat-suppressed 3-dimensional controlled aliasing in parallel imaging results in higher acceleration sampling perfection with application optimized contrast using different flip angle evolutions MRI of the knee in adults." British Journal of Radiology 93, no. 1112 (August 2020): 20190725. http://dx.doi.org/10.1259/bjr.20190725.

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Objective: To compare htree-dimensional CAIPIRINHA SPACE and two-dimensional turbo spin echo (2D TSE) MRI in the diagnosis of knee pathology in symptomatic adult patients. Methods: From February to September in 2018, 120 patients who underwent a knee MRI using both 3D CAIPIRINHA SPACE and 2D TSE MRI were enrolled. The signal-to-noise ratios (SNRs) and contrast-to-noise ratio (CNR) of the 2D and 3D MRI were compared using a paired t-test. Two radiologists independently evaluated both 2D and 3D MRI images using scoring systems for the menisci, ligaments, and cartilage. Intermethod, inter- and intrareader agreements were determined using an intraclass correlation coefficient (ICC). The diagnostic performance of both methods was measured in 44 patients with arthroscopy. Results: The mean scan time of 3D CAIPIRINHA SPACE MRI (4’ 43”) was shorter than that of 2D TSE MRI (17’ 27”). The mean SNR and CNR of 3D CAIPIRINHA SPACE was higher than those of 2D TSE MRI (mean difference, 3.97 of SNR and 1.58 of CNR; p < 0.001 and p = .038, respectively). Intermethod (ICC, 0.84–1.0) and inter-reader (ICC, 0.75–0.97), and intra-reader agreements (ICC, 0.87–1.0) were good or excellent. The diagnostic accuracy of 3D CAIPIRINHA SPACE sequence was equal for ligament (95.5%) and better for meniscal and cartilage evaluation (84.1% each), compared to 2D TSE MRI (79.5% each). Conclusion: The fat-suppressed 3D CAIPIRINHA SPACE MRI maybe useful in clinical practice for the evaluation of the knee in place of the 2D conventional MRI protocol. Advances in knowledge: 1. The 3D CAIPIRINHA SPACE MRI of the knee joint may be acceptable to be used in clinical practice showing comparable imaging quality compared to conventional 2D TSE MRI. 2. Compared with arthroscopic findings as the gold-standard, the diagnostic performance of 3D CAIPIRINHA SPACE MRI was equal or better for knee joint evaluation than that of 2D TSE MRI, as well as with shorter scan time.
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Books on the topic "HTREK-1"

1

Weygandt, Jerry J. Accounting Principles with CD 6e Volume 1 and Peac Htree Complete Accounting Set. John Wiley & Sons Inc, 2001.

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