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MTSET modification of D4S6 cysteines stabilize the fast inactivated state of Nav1.5 sodium channels.

Frontiers in pharmacology

O'Leary ME, Chahine M.
PMID: 26150789
Front Pharmacol. 2015 Jun 19;6:118. doi: 10.3389/fphar.2015.00118. eCollection 2015.

The transmembrane S6 segments of Na(+) sodium channels form the cytoplasmic entrance of the channel and line the internal aspects of the aqueous pore. This region of the channel has been implicated in Na(+) channel permeation, gating, and pharmacology....

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O'Leary ME, Chahine M. MTSET modification of D4S6 cysteines stabilize the fast inactivated state of Nav1.5 sodium channels. Front Pharmacol. 2015;6:118doi: 10.3389/fphar.2015.00118.
O'Leary, M. E., & Chahine, M. (2015). MTSET modification of D4S6 cysteines stabilize the fast inactivated state of Nav1.5 sodium channels. Frontiers in pharmacology, 6118. https://doi.org/10.3389/fphar.2015.00118
O'Leary, Michael E, and Chahine, Mohamed. "MTSET modification of D4S6 cysteines stabilize the fast inactivated state of Nav1.5 sodium channels." Frontiers in pharmacology vol. 6 (2015): 118. doi: https://doi.org/10.3389/fphar.2015.00118
O'Leary ME, Chahine M. MTSET modification of D4S6 cysteines stabilize the fast inactivated state of Nav1.5 sodium channels. Front Pharmacol. 2015 Jun 19;6:118. doi: 10.3389/fphar.2015.00118. eCollection 2015. PMID: 26150789; PMCID: PMC4472985.
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Neuroprotection for acute optic neuritis-Can it work?.

Multiple sclerosis and related disorders

Raftopoulos RE, Kapoor R.
PMID: 25877841
Mult Scler Relat Disord. 2013 Oct;2(4):307-11. doi: 10.1016/j.msard.2013.02.001. Epub 2013 Mar 13.

Optic neuritis is a common manifestation of MS and the acute inflammatory lesion in the optic nerve resembles demyelinating plaques elsewhere in the CNS. As with other MS relapses, treatment with corticosteroids has little or no impact on the...

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Raftopoulos RE, Kapoor R. Neuroprotection for acute optic neuritis-Can it work?. Mult Scler Relat Disord. 2013;2(4):307-11doi: 10.1016/j.msard.2013.02.001.
Raftopoulos, R. E., & Kapoor, R. (2013). Neuroprotection for acute optic neuritis-Can it work?. Multiple sclerosis and related disorders, 2(4), 307-11. https://doi.org/10.1016/j.msard.2013.02.001
Raftopoulos, R E, and Kapoor, R. "Neuroprotection for acute optic neuritis-Can it work?." Multiple sclerosis and related disorders vol. 2,4 (2013): 307-11. doi: https://doi.org/10.1016/j.msard.2013.02.001
Raftopoulos RE, Kapoor R. Neuroprotection for acute optic neuritis-Can it work?. Mult Scler Relat Disord. 2013 Oct;2(4):307-11. doi: 10.1016/j.msard.2013.02.001. Epub 2013 Mar 13. PMID: 25877841.
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Axonal Membranes and Their Domains: Assembly and Function of the Axon Initial Segment and Node of Ranvier.

Frontiers in cellular neuroscience

Nelson AD, Jenkins PM.
PMID: 28536506
Front Cell Neurosci. 2017 May 09;11:136. doi: 10.3389/fncel.2017.00136. eCollection 2017.

Neurons are highly specialized cells of the nervous system that receive, process and transmit electrical signals critical for normal brain function. Here, we review the intricate organization of axonal membrane domains that facilitate rapid action potential conduction underlying communication...

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Nelson AD, Jenkins PM. Axonal Membranes and Their Domains: Assembly and Function of the Axon Initial Segment and Node of Ranvier. Front Cell Neurosci. 2017;11:136doi: 10.3389/fncel.2017.00136.
Nelson, A. D., & Jenkins, P. M. (2017). Axonal Membranes and Their Domains: Assembly and Function of the Axon Initial Segment and Node of Ranvier. Frontiers in cellular neuroscience, 11136. https://doi.org/10.3389/fncel.2017.00136
Nelson, Andrew D, and Jenkins, Paul M. "Axonal Membranes and Their Domains: Assembly and Function of the Axon Initial Segment and Node of Ranvier." Frontiers in cellular neuroscience vol. 11 (2017): 136. doi: https://doi.org/10.3389/fncel.2017.00136
Nelson AD, Jenkins PM. Axonal Membranes and Their Domains: Assembly and Function of the Axon Initial Segment and Node of Ranvier. Front Cell Neurosci. 2017 May 09;11:136. doi: 10.3389/fncel.2017.00136. eCollection 2017. PMID: 28536506; PMCID: PMC5422562.
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Prostasin: An Epithelial Sodium Channel Regulator.

Journal of biomarkers

Aggarwal S, Dabla PK, Arora S.
PMID: 26317012
J Biomark. 2013;2013:179864. doi: 10.1155/2013/179864. Epub 2013 Jul 02.

Prostasin is a glycophosphatidylinositol-anchored protein which is found in prostate gland, kidney, bronchi, colon, liver, lung, pancreas, and salivary glands. It is a serine protease with trypsin-like substrate specificity which was first purified from seminal fluid in 1994. In...

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Aggarwal S, Dabla PK, Arora S. Prostasin: An Epithelial Sodium Channel Regulator. J Biomark. 2013;2013:179864doi: 10.1155/2013/179864.
Aggarwal, S., Dabla, P. K., & Arora, S. (2013). Prostasin: An Epithelial Sodium Channel Regulator. Journal of biomarkers, 2013179864. https://doi.org/10.1155/2013/179864
Aggarwal, Shakti, et al. "Prostasin: An Epithelial Sodium Channel Regulator." Journal of biomarkers vol. 2013 (2013): 179864. doi: https://doi.org/10.1155/2013/179864
Aggarwal S, Dabla PK, Arora S. Prostasin: An Epithelial Sodium Channel Regulator. J Biomark. 2013;2013:179864. doi: 10.1155/2013/179864. Epub 2013 Jul 02. PMID: 26317012; PMCID: PMC4436870.
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High-content screening identifies a role for Na(+) channels in insulin production.

Royal Society open science

Szabat M, Modi H, Ramracheya R, Girbinger V, Chan F, Lee JT, Piske M, Kamal S, Carol Yang YH, Welling A, Rorsman P, Johnson JD.
PMID: 27019722
R Soc Open Sci. 2015 Dec 02;2(12):150306. doi: 10.1098/rsos.150306. eCollection 2015 Dec.

Insulin production is the central feature of functionally mature and differentiated pancreatic β-cells. Reduced insulin transcription and dedifferentiation have been implicated in type 2 diabetes, making drugs that could reverse these processes potentially useful. We have previously established ratiometric...

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Szabat M, Modi H, Ramracheya R, et al. High-content screening identifies a role for Na(+) channels in insulin production. R Soc Open Sci. 2015;2(12):150306doi: 10.1098/rsos.150306.
Szabat, M., Modi, H., Ramracheya, R., Girbinger, V., Chan, F., Lee, J. T., Piske, M., Kamal, S., Carol Yang, Y. H., Welling, A., Rorsman, P., & Johnson, J. D. (2015). High-content screening identifies a role for Na(+) channels in insulin production. Royal Society open science, 2(12), 150306. https://doi.org/10.1098/rsos.150306
Szabat, Marta, et al. "High-content screening identifies a role for Na(+) channels in insulin production." Royal Society open science vol. 2,12 (2015): 150306. doi: https://doi.org/10.1098/rsos.150306
Szabat M, Modi H, Ramracheya R, Girbinger V, Chan F, Lee JT, Piske M, Kamal S, Carol Yang YH, Welling A, Rorsman P, Johnson JD. High-content screening identifies a role for Na(+) channels in insulin production. R Soc Open Sci. 2015 Dec 02;2(12):150306. doi: 10.1098/rsos.150306. eCollection 2015 Dec. PMID: 27019722; PMCID: PMC4807443.
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Stepping Out of the Shade: Control of Neuronal Activity by the Scaffold Protein Kidins220/ARMS.

Frontiers in cellular neuroscience

Scholz-Starke J, Cesca F.
PMID: 27013979
Front Cell Neurosci. 2016 Mar 14;10:68. doi: 10.3389/fncel.2016.00068. eCollection 2016.

The correct functioning of the nervous system depends on the exquisitely fine control of neuronal excitability and synaptic plasticity, which relies on an intricate network of protein-protein interactions and signaling that shapes neuronal homeostasis during development and in adulthood....

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Scholz-Starke J, Cesca F. Stepping Out of the Shade: Control of Neuronal Activity by the Scaffold Protein Kidins220/ARMS. Front Cell Neurosci. 2016;10:68doi: 10.3389/fncel.2016.00068.
Scholz-Starke, J., & Cesca, F. (2016). Stepping Out of the Shade: Control of Neuronal Activity by the Scaffold Protein Kidins220/ARMS. Frontiers in cellular neuroscience, 1068. https://doi.org/10.3389/fncel.2016.00068
Scholz-Starke, Joachim, and Cesca, Fabrizia. "Stepping Out of the Shade: Control of Neuronal Activity by the Scaffold Protein Kidins220/ARMS." Frontiers in cellular neuroscience vol. 10 (2016): 68. doi: https://doi.org/10.3389/fncel.2016.00068
Scholz-Starke J, Cesca F. Stepping Out of the Shade: Control of Neuronal Activity by the Scaffold Protein Kidins220/ARMS. Front Cell Neurosci. 2016 Mar 14;10:68. doi: 10.3389/fncel.2016.00068. eCollection 2016. PMID: 27013979; PMCID: PMC4789535.
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Current View in Platinum Drug Mechanisms of Peripheral Neurotoxicity.

Toxics

Chiorazzi A, Semperboni S, Marmiroli P.
PMID: 29051466
Toxics. 2015 Aug 07;3(3):304-321. doi: 10.3390/toxics3030304.

Peripheral neurotoxicity is the dose-limiting factor for clinical use of platinum derivatives, a class of anticancer drugs which includes cisplatin, carboplatin, and oxaliplatin. In particular cisplatin and oxaliplatin induce a severe peripheral neurotoxicity while carboplatin is less neurotoxic. The...

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Chiorazzi A, Semperboni S, Marmiroli P. Current View in Platinum Drug Mechanisms of Peripheral Neurotoxicity. Toxics. 2015;3(3):304-321doi: 10.3390/toxics3030304.
Chiorazzi, A., Semperboni, S., & Marmiroli, P. (2015). Current View in Platinum Drug Mechanisms of Peripheral Neurotoxicity. Toxics, 3(3), 304-321. https://doi.org/10.3390/toxics3030304
Chiorazzi, Alessia, et al. "Current View in Platinum Drug Mechanisms of Peripheral Neurotoxicity." Toxics vol. 3,3 (2015): 304-321. doi: https://doi.org/10.3390/toxics3030304
Chiorazzi A, Semperboni S, Marmiroli P. Current View in Platinum Drug Mechanisms of Peripheral Neurotoxicity. Toxics. 2015 Aug 07;3(3):304-321. doi: 10.3390/toxics3030304. PMID: 29051466; PMCID: PMC5606682.
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ProNGF derived from rat sciatic nerves downregulates neurite elongation and axon specification in PC12 cells.

Frontiers in cellular neuroscience

Trigos AS, Longart M, García L, Castillo C, Forsyth P, Medina R.
PMID: 26441535
Front Cell Neurosci. 2015 Sep 15;9:364. doi: 10.3389/fncel.2015.00364. eCollection 2015.

Several reports have shown that a sciatic nerve conditioned media (CM) causes neuronal-like differentiation in PC12 cells. This differentiation is featured by neurite outgrowth, which are exclusively dendrites, without axon or sodium current induction. In previous studies, our group...

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Trigos AS, Longart M, García L, et al. ProNGF derived from rat sciatic nerves downregulates neurite elongation and axon specification in PC12 cells. Front Cell Neurosci. 2015;9:364doi: 10.3389/fncel.2015.00364.
Trigos, A. S., Longart, M., García, L., Castillo, C., Forsyth, P., & Medina, R. (2015). ProNGF derived from rat sciatic nerves downregulates neurite elongation and axon specification in PC12 cells. Frontiers in cellular neuroscience, 9364. https://doi.org/10.3389/fncel.2015.00364
Trigos, Anna Sofía, et al. "ProNGF derived from rat sciatic nerves downregulates neurite elongation and axon specification in PC12 cells." Frontiers in cellular neuroscience vol. 9 (2015): 364. doi: https://doi.org/10.3389/fncel.2015.00364
Trigos AS, Longart M, García L, Castillo C, Forsyth P, Medina R. ProNGF derived from rat sciatic nerves downregulates neurite elongation and axon specification in PC12 cells. Front Cell Neurosci. 2015 Sep 15;9:364. doi: 10.3389/fncel.2015.00364. eCollection 2015. PMID: 26441535; PMCID: PMC4569732.
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SCN1A and SCN1B gene polymorphisms and their association with plasma concentrations of carbamazepine and carbamazepine 10, 11 epoxide in Iranian epileptic patients.

Iranian journal of basic medical sciences

Namazi S, Azarpira N, Javidnia K, Emami M, Rahjoo R, Berahmand R, Borhani-Haghighi A.
PMID: 26877851
Iran J Basic Med Sci. 2015 Dec;18(12):1215-20.

OBJECTIVE S: From a genetic point of view, epilepsy is a polygenic multifactorial syndrome. The SCN1A and B genes belong to a family of genes that provide instructions for making sodium channels. Understanding the relevance of SCN1A and SCN1B...

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Namazi S, Azarpira N, Javidnia K, et al. SCN1A and SCN1B gene polymorphisms and their association with plasma concentrations of carbamazepine and carbamazepine 10, 11 epoxide in Iranian epileptic patients. Iran J Basic Med Sci. 2015;18(12):1215-20
Namazi, S., Azarpira, N., Javidnia, K., Emami, M., Rahjoo, R., Berahmand, R., & Borhani-Haghighi, A. (2015). SCN1A and SCN1B gene polymorphisms and their association with plasma concentrations of carbamazepine and carbamazepine 10, 11 epoxide in Iranian epileptic patients. Iranian journal of basic medical sciences, 18(12), 1215-20.
Namazi, Soha, et al. "SCN1A and SCN1B gene polymorphisms and their association with plasma concentrations of carbamazepine and carbamazepine 10, 11 epoxide in Iranian epileptic patients." Iranian journal of basic medical sciences vol. 18,12 (2015): 1215-20.
Namazi S, Azarpira N, Javidnia K, Emami M, Rahjoo R, Berahmand R, Borhani-Haghighi A. SCN1A and SCN1B gene polymorphisms and their association with plasma concentrations of carbamazepine and carbamazepine 10, 11 epoxide in Iranian epileptic patients. Iran J Basic Med Sci. 2015 Dec;18(12):1215-20. PMID: 26877851; PMCID: PMC4744361.
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Conduction abnormalities and ventricular arrhythmogenesis: The roles of sodium channels and gap junctions.

International journal of cardiology. Heart & vasculature

Tse G, Yeo JM.
PMID: 26839915
Int J Cardiol Heart Vasc. 2015 Dec 07;9:75-82. doi: 10.1016/j.ijcha.2015.10.003.

Ventricular arrhythmias arise from disruptions in the normal orderly sequence of electrical activation and recovery of the heart. They can be categorized into disorders affecting predominantly cellular depolarization or repolarization, or those involving action potential (AP) conduction. This article...

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Tse G, Yeo JM. Conduction abnormalities and ventricular arrhythmogenesis: The roles of sodium channels and gap junctions. Int J Cardiol Heart Vasc. 2015;9:75-82doi: 10.1016/j.ijcha.2015.10.003.
Tse, G., & Yeo, J. M. (2015). Conduction abnormalities and ventricular arrhythmogenesis: The roles of sodium channels and gap junctions. International journal of cardiology. Heart & vasculature, 975-82. https://doi.org/10.1016/j.ijcha.2015.10.003
Tse, Gary, and Yeo, Jie Ming. "Conduction abnormalities and ventricular arrhythmogenesis: The roles of sodium channels and gap junctions." International journal of cardiology. Heart & vasculature vol. 9 (2015): 75-82. doi: https://doi.org/10.1016/j.ijcha.2015.10.003
Tse G, Yeo JM. Conduction abnormalities and ventricular arrhythmogenesis: The roles of sodium channels and gap junctions. Int J Cardiol Heart Vasc. 2015 Dec 07;9:75-82. doi: 10.1016/j.ijcha.2015.10.003. PMID: 26839915; PMCID: PMC4695916.
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Local anaesthetic use in cancer surgery and disease recurrence: role of voltage-gated sodium channels? British Journal of Anaesthesia, 2015; 113(6): 899-902, DOI 10.1093/bja/aeu221.

British journal of anaesthesia

[No authors listed]
PMID: 25904641
Br J Anaesth. 2015 Jun;114(6):1014. doi: 10.1093/bja/aev139. Epub 2015 Apr 22.

In the original article, under the "Declaration of Interests" section, the authors stated "none declared" since they had no direct interest in the use of local anaesthetics to treat cancer (the focus of the article being the beneficial use...

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Local anaesthetic use in cancer surgery and disease recurrence: role of voltage-gated sodium channels? British Journal of Anaesthesia, 2015; 113(6): 899-902, DOI 10.1093/bja/aeu221. Br J Anaesth. 2015;114(6):1014doi: 10.1093/bja/aev139.
(2015). Local anaesthetic use in cancer surgery and disease recurrence: role of voltage-gated sodium channels? British Journal of Anaesthesia, 2015; 113(6): 899-902, DOI 10.1093/bja/aeu221. British journal of anaesthesia, 114(6), 1014. https://doi.org/10.1093/bja/aev139
"Local anaesthetic use in cancer surgery and disease recurrence: role of voltage-gated sodium channels? British Journal of Anaesthesia, 2015; 113(6): 899-902, DOI 10.1093/bja/aeu221." British journal of anaesthesia vol. 114,6 (2015): 1014. doi: https://doi.org/10.1093/bja/aev139
Local anaesthetic use in cancer surgery and disease recurrence: role of voltage-gated sodium channels? British Journal of Anaesthesia, 2015; 113(6): 899-902, DOI 10.1093/bja/aeu221. Br J Anaesth. 2015 Jun;114(6):1014. doi: 10.1093/bja/aev139. Epub 2015 Apr 22. PMID: 25904641.
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Changes in urinary excretion of water and sodium transporters during amiloride and bendroflumethiazide treatment.

World journal of nephrology

Jensen JM, Mose FH, Kulik AE, Bech JN, Fenton RA, Pedersen EB.
PMID: 26167467
World J Nephrol. 2015 Jul 06;4(3):423-37. doi: 10.5527/wjn.v4.i3.423.

AIM: To quantify changes in urinary excretion of aquaporin2 water channels (u-AQP2), the sodium-potassium-chloride co-transporter (u-NKCC2) and the epithelial sodium channels (u-ENaC) during treatment with bendroflumethiazide (BFTZ), amiloride and placebo.METHODS: In a randomized, double-blinded, placebo-controlled, 3-way crossover study we...

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Jensen JM, Mose FH, Kulik AE, et al. Changes in urinary excretion of water and sodium transporters during amiloride and bendroflumethiazide treatment. World J Nephrol. 2015;4(3):423-37doi: 10.5527/wjn.v4.i3.423.
Jensen, J. M., Mose, F. H., Kulik, A. E., Bech, J. N., Fenton, R. A., & Pedersen, E. B. (2015). Changes in urinary excretion of water and sodium transporters during amiloride and bendroflumethiazide treatment. World journal of nephrology, 4(3), 423-37. https://doi.org/10.5527/wjn.v4.i3.423
Jensen, Janni M, et al. "Changes in urinary excretion of water and sodium transporters during amiloride and bendroflumethiazide treatment." World journal of nephrology vol. 4,3 (2015): 423-37. doi: https://doi.org/10.5527/wjn.v4.i3.423
Jensen JM, Mose FH, Kulik AE, Bech JN, Fenton RA, Pedersen EB. Changes in urinary excretion of water and sodium transporters during amiloride and bendroflumethiazide treatment. World J Nephrol. 2015 Jul 06;4(3):423-37. doi: 10.5527/wjn.v4.i3.423. PMID: 26167467; PMCID: PMC4491934.
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Showing 1 to 12 of 567 entries