Results 41 to 50 of about 3,466 (187)

Возможная физиологическая функция эндогенного уабаина

Интегративная физиология, 2021
Наши результаты свидетельствуют о том, что эндогенный уабаин запускает два разных сигнальных процесса. Первый, быстрый процесс, приводит к модуляции активационного воротного устройства каналов NaV1.8, что снижает их функциональную активность.
Валентина Альбертовна Пеннияйнен, Вера Борисовна Плахова, Светлана Александровна Подзорова, Станислав Георгиевич Терехин, Борис Владимирович Крылов   +4 more
doaj   +1 more source

Differential regulation of bladder pain and voiding function by sensory afferent populations revealed by selective optogenetic activation [PDF]

, 2010
Bladder-innervating primary sensory neurons mediate reflex-driven bladder function under normal conditions, and contribute to debilitating bladder pain and/or overactivity in pathological states. The goal of this study was to examine the respective roles
DeBerry, Jennifer J, Samineni, Vijay K, Copits, Bryan A, Sullivan, Christopher J, Vogt, Sherri K, Albers, Kathryn M, Davis, Brian M, Gereau, Robert W, IV   +7 more
core   +4 more sources

Generation of induced pluripotent stem cells (iPSCs) from an infant with catecholaminergic polymorphic ventricular tachycardia carrying the double heterozygous mutations A1855D in RyR2 and Q1362H in SCN10A

Stem Cell Research, 2019
Induced pluripotent stem cells (iPSCs) were generated from peripheral blood mononuclear cells (PBMCs) isolated from the peripheral blood of a 4 month-old boy with catecholaminergic polymorphic ventricular tachycardia carrying the double heterozygous ...
Yanmin Zhang, Anmao Li, Christopher L.-H. Huang, Guoxia Wang, Danying Wang   +4 more
doaj   +1 more source

A variant in the SCN10A enhancer may affect human mechanical pain sensitivity [PDF]

Molecular Pain, 2018
Expression of Nav1.8, encoded by SCN10A, can affect pain transmission and thus mediate the human pain phenotype. In the current study, we assessed whether the variant rs6801957, located in the SCN10A enhancer region, may have the potential to affect human pain. Through dual-luciferase reporter assays in 293T cells, we found that the SCN10A enhancer A (
Duan, Guangyou, Sun, Jiaoli, Li, Ningbo, Zheng, Hua, Guo, Shanna, Zhang, Yuhao, Wang, Qingli, Ying, Ying, Zhang, Mi, Huang, Penghao, Zhang, Xianwei   +10 more
openaire   +2 more sources

Nav1.7 and other voltage-gated sodium channels as drug targets for pain relief [PDF]

, 2016
INTRODUCTION: Chronic pain is a massive clinical problem. We discuss the potential of subtype selective sodium channel blockers that may provide analgesia with limited side effects.
Emery, EC, Luiz, AP, Wood, JN
core   +1 more source

The Potential Effect of Nav1.8 in Autism Spectrum Disorder: Evidence From a Congenital Case With Compound Heterozygous SCN10A Mutations

Frontiers in Molecular Neuroscience, 2021
Apart from the most prominent symptoms in Autism spectrum disorder (ASD), namely deficits in social interaction, communication and repetitive behavior, patients often show abnormal sensory reactivity to environmental stimuli.
Björn Heinrichs, Baowen Liu, Baowen Liu, Jin Zhang, Jannis E. Meents, Kim Le, Andelain Erickson, Petra Hautvast, Xiwen Zhu, Ningbo Li, Yi Liu, Yi Liu, Marc Spehr, Ute Habel, Ute Habel, Markus Rothermel, Barbara Namer, Xianwei Zhang, Angelika Lampert, Guangyou Duan   +19 more
doaj   +1 more source

Whither Art Thou, SCN10A, and What Art Thou Doing? [PDF]

Circulation Research, 2012
Since its initial cloning in 1992, SCN5A (Nav1.5) has become known as “the” cardiac sodium channel.1 SCN5A encodes a tetrodotoxin (TTX)-resistant channel that is responsible for the inward sodium current (INa), which initiates the cardiac action potential.
openaire   +2 more sources

Integration of genetics into a systems model of electrocardiographic traits using humanCVD BeadChip [PDF]

, 2012
<p>Background—Electrocardiographic traits are important, substantially heritable determinants of risk of arrhythmias and sudden cardiac death.</p> <p>Methods and Results—In this study, 3 population-based cohorts (n=10 526) genotyped ...
Adeniran, I., Amuzu, A., Braund, P.S., Burton, P.R., Casas, J.-P., Day, I.N.M., Drenos, F., Eriksson, P., Folkersen, L., Gaunt, T.R., Hancox, J.C., Hingorani, A.D., Humphries, S.E., Kivimaki, M., Kumari, M., Lawlor, D.A., Macfarlane, P.W., Nelson, C.P., Samani, N.J., Shah, S., Talmud, P.J., Tobin, M.D., Tomaszewski, M., Whittaker, J., Zhang, H.   +24 more
core   +1 more source

Genetics update: monogenetics, polygene disorders and the quest for modifying genes [PDF]

, 2018
The genetic channelopathies are a broad collection of diseases. Many ion channel genes demonstrate wide phenotypic pleiotropy, but nonetheless concerted efforts have been made to characterise genotype-phenotype relationships.
Symonds, Joseph D., Zuberi, Sameer M.
core   +1 more source

Electrophysiological Mechanisms of Brugada Syndrome: Insights from Pre-clinical and Clinical Studies. [PDF]

, 2016
This is the final version of the article. It first appeared from Frontiers via https://doi.org/10.3389/fphys.2016.00467Brugada syndrome (BrS), is a primary electrical disorder predisposing affected individuals to sudden cardiac death via the development ...
Chan, Yin WF, Keung, Wendy, Laxton, Victoria, Li, Ka HC, Li, Ronald A, Liu, Tong, Tse, Gary, Yan, Bryan P   +7 more
core   +5 more sources