Search results for: gated
#33108349 2020/10/27 To Up
MIR448 antagomir reduces arrhythmic risk after myocardial infarction by upregulating the cardiac sodium channel.Cardiac ischemia is associated with arrhythmias, but effective therapies are limited. The cardiac voltage gated sodium channel α-subunit (SCN5A), encoding the Nav1.5 current, plays a key role in the cardiac electrical conduction and arrhythmic risk. Here, we show that hypoxia reduces Nav1.5 through effects on a microRNA (miR), miR-448. The expression of miR-448 is increased in ischemic cardiomyopathy. miR-448 has a conserved binding site in 3'-UTR of SCN5A. miR-448 binding to this site suppressed SCN5A expression and sodium currents. Hypoxia-induced HIF1α and NF-κB were major transcriptional regulators for MIR448. Hypoxia also relieved MIR448 transcriptional suppression by RE1 silencing transcription factor (REST). Inhibition of miR-448 reduced arrhythmic risk after myocardial infarction. These results indicated that ischemia drove miR-448 expression, reduced Nav1.5 current and increased arrhythmic risk. Arrhythmic risk was improved by preventing Nav1.5 downregulation, suggesting a new approach to antiarrhythmic therapy.
Gyeoung-Jin Kang, An Xie, Hong Liu, Samuel C Dudley
2751 related Products with: MIR448 antagomir reduces arrhythmic risk after myocardial infarction by upregulating the cardiac sodium channel.1 mg 1 G5 MG 1KG 1KG500 tests1.00 flask 5 G100ug Lyophilized 1 G200 units
Error loading info... Pleas try again later.
#33106102 2020/10/26 To Up
Voltage-Gated Calcium Channels in Nonexcitable Tissues.The identification of a gain-of-function mutation in as the cause of Timothy syndrome, a rare disorder characterized by cardiac arrhythmias and syndactyly, highlighted roles for the L-type voltage-gated Ca channel Ca1.2 in nonexcitable cells. Previous studies in cells and animal models had suggested that several voltage-gated Ca channels (VGCCs) regulated critical signaling events in various cell types that are not expected to support action potential, but definitive data were lacking. VGCCs occupy a special position among ion channels, uniquely able to translate membrane excitability into the cytoplasmic Ca changes that underlie the cellular responses to electrical activity. Yet how these channels function in cells not firing action potentials and what the consequences of their actions are in nonexcitable cells remain critical questions. The development of new animal and cellular models and the emergence of large data sets and unbiased genome screens have added to our understanding of the unanticipated roles for VGCCs in nonexcitable cells. Here, we review current knowledge of VGCC regulation and function in nonexcitable tissues and cells, with the goal of providing a platform for continued investigation. Expected final online publication date for the , Volume 83 is February 10, 2021. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
Geoffrey S Pitt, Maiko Matsui, Chike Cao100ug100ug
#33105687 2020/10/22 To Up
Comparison of the Productivity of Primiparous Sows Housed in Individual Stalls and Group Housing Systems.This study was conducted to provide commercial pig farms with information about group housing systems for sows in accordance with the amendment of the prohibition law for individual stalls for sows in South Korea. Therefore, this experiment was performed to compare the effects of individual stalls (IS) and group housing systems (GS) on the productivity of sows to investigate the feasibility of replacing individual stalls with group housing systems in commercial sow units. Forty primiparous sows (Landrace × Yorkshire; 210.67 ± 2.22 kg average initial body weight) were randomly assigned to four treatments with restricted feeding after 8 weeks from artificial insemination. The four treatments were (i) individual stalls (IS; housed in pen stalls), (ii) short stalls (SS; sows housed in pens with non-gated feeding stalls), (iii) free access stalls (FAS; a non-competitive housing system), and (iv) electronic sow feeders (ESF; used with radio frequency identification technology to allow individual sow management without individual confinement). All sows were transferred to farrowing crates at 110 days of gestation. There were no differences in sow productive performance, reproductive performance, and colostrum composition between IS and GS and among GS. The considered GS did not negatively affect any productivity parameters of primiparous sows compared with IS; the GS could replace IS in commercial sow units.
Yejin Min, Yohan Choi, Joeun Kim, Doowan Kim, Yongdae Jeong, Younghwa Kim, Minho Song, Hyunjung Jung
2435 related Products with: Comparison of the Productivity of Primiparous Sows Housed in Individual Stalls and Group Housing Systems.15ml1000 pcs2000 pcs
#33105624 2020/10/22 To Up
Constitutive Genetic Deletion of Increases Alcohol Preference during Adolescence.The hyperpolarization-activated cyclic nucleotide-gated channel (HCN), which underlies the hyperpolarization-activated cation current (I), has diverse roles in regulating neuronal excitability across cell types and brain regions. Recently, HCN channels have been implicated in preclinical models of substance abuse including alcohol. In the prefrontal cortex of rodents, HCN expression and I magnitude are developmentally regulated during adolescence and may be vulnerable to alcohol's effects. In mice, binge alcohol consumption during the adolescent period results in a sustained reduction in I that coincides with increased alcohol consumption in adulthood, yet the direct role HCN channels have on alcohol consumption are unknown. Here, we show that the genetic deletion of causes an increase in alcohol preference on intermittent 2-bottle choice task in homozygous null (HCN1) male mice compared to wild-type littermates without affecting saccharine or quinine preference. The targeted viral deletion of HCN1 in pyramidal neurons of the medial prefrontal cortex resulted in a gradual loss of expression and a reduction in I magnitude during adolescence, however, this did not significantly affect alcohol consumption or preference. We conclude that while HCN1 regulates alcohol preference, the genetic deletion of in the medial prefrontal cortex does not appear to be the locus for this effect.
Michael C Salling, Neil L Harrison
2890 related Products with: Constitutive Genetic Deletion of Increases Alcohol Preference during Adolescence.25 G 25 G 500 ml 100ug100 tests 25 G5 g 5 G100 1 ml 500 ml 100 g
Error loading info... Pleas try again later.
#33104294 2020/10/26 To Up
Reduction of breathing artifacts in multifrequency magnetic resonance elastography of the abdomen.With abdominal magnetic resonance elastography (MRE) often suffering from breathing artifacts, it is recommended to perform MRE during breath-hold. However, breath-hold acquisition prohibits extended multifrequency MRE examinations and yields inconsistent results when patients cannot hold their breath. The purpose of this work was to analyze free-breathing strategies in multifrequency MRE of abdominal organs.
Mehrgan Shahryari, Tom Meyer, Carsten Warmuth, Helge Herthum, Gergely Bertalan, Heiko Tzschätzsch, Lisa Stencel, Steffen Lukas, Ledia Lilaj, Jürgen Braun, Ingolf Sack
2281 related Products with: Reduction of breathing artifacts in multifrequency magnetic resonance elastography of the abdomen.5 G1100 μg100 µl (2 mM)
No related Items
#33103452 2020/10/26 To Up
AMPK mediates regulation of voltage-gated calcium channels by leptin in orexigenic neurons from arcuate nucleus.Neuronal control of the energy homeostasis requires the arcuate nucleus of hypothalamus. This structure integrates peripheral and central signals concerning the energy state of the body. It is comprised of two populations of neurons releasing anorexigenic and orexigenic peptides amongst others. Both populations are regulated by leptin, an anorexigenic hormone released by white adipose tissue. Voltage-gated calcium entry is critical to promote neurotransmitter and hormone release. It is already known that calcium channel current is inhibited by leptin in orexigenic neurons. However, fine-tuning details of calcium channel regulation in arcuate nucleus by leptin remain to be elucidated. This work aimed to investigate whether AMPK underlies the leptin-induced inhibition of calcium channels. By using patch-clamping methods, immunocytochemical and biochemical reagents we recorded calcium channel currents in orexigenic NPY neurons of arcuate nucleus of the rat. Consistently, leptin inhibition of the calcium channel current not only was prevented by AMPK inhibition with Compound C but also was hampered with AICAR. Furthermore, leptin inhibited selectively L-type calcium channel current amplitude without major changes in voltage dependence or current kinetics. These results support for the first time a key role of AMPK in the maintenance and regulation of the voltage-gated calcium channels. Together, they advance our understanding of the regulation of calcium channels in central nervous system and emerging questions concerning food intake and energy balance.
Karina Bermeo, Hector Castro, Isabel Arenas, David E Garcia
1220 related Products with: AMPK mediates regulation of voltage-gated calcium channels by leptin in orexigenic neurons from arcuate nucleus.100ug 100ul2 Pieces/Box100 μg100ug96 tests100ug300 units100ug2 Pieces/Box96 wells
#33101845 2020/09/21 To Up
An Unorthodox Mechanism Underlying Voltage Sensitivity of TRPV1 Ion Channel.While the capsaicin receptor transient receptor potential vanilloid 1 (TRPV1) channel is a polymodal nociceptor for heat, capsaicin, and protons, the channel's responses to each of these stimuli are profoundly regulated by membrane potential, damping or even prohibiting its response at negative voltages and amplifying its response at positive voltages. Therefore, voltage sensitivity of TRPV1 is anticipated to play an important role in shaping pain responses. How voltage regulates TRPV1 activation remains unknown. Here, it is shown that voltage sensitivity does not originate from the S4 segment like classic voltage-gated ion channels; instead, outer pore acidic residues directly partake in voltage-sensitive activation, with their negative charges collectively constituting the observed gating charges. Outer pore gating-charge movement is titratable by extracellular pH and is allosterically coupled to channel activation, likely by influencing the upper gate in the ion selectivity filter. Elucidating this unorthodox voltage-gating process provides a mechanistic foundation for understanding TRPV1 polymodal gating and opens the door to novel approaches regulating channel activity for pain management.
Fan Yang, Lizhen Xu, Bo Hyun Lee, Xian Xiao, Vladimir Yarov-Yarovoy, Jie Zheng
1060 related Products with: An Unorthodox Mechanism Underlying Voltage Sensitivity of TRPV1 Ion Channel.100ug100ug 100ul100ug Lyophilized0.1ml (1mg/ml)100ug Lyophilized100ug Lyophilized100ug Lyophilized1100ug Lyophilized100ug Lyophilized5mg
#33101018 2020/09/25 To Up
Editorial: From Peptide and Protein Toxins to Ion Channel Structure/Function and Drug Design.
Annette Nicke, Chris Ulens, Jean-Francois Rolland, Victor I Tsetlin
1007 related Products with: Editorial: From Peptide and Protein Toxins to Ion Channel Structure/Function and Drug Design.1000 TESTS/0.65ml100ul 5 G2.5 mg1 ml100 100ul480/kit10 mg
No related Items
Voortstraat 49, 1910 Kampenhout BELGIUM
Tel 0032 16 58 90 45 Fax 0032 16 50 90 45
9, rue Lagrange, 75005 Paris
Tel 01 43 25 01 50 Fax 01 43 25 01 60
52062 Aachen Deutschland
Tel 0241 40 08 90 86 Fax 0241 55 91 05 36
Howard Frank Turnberry House
1404-1410 High Road
Whetstone London N20 9BH
Tel 020 3393 8531 Fax 020 8445 9411
Schweiz Züri +41435006251
Česká republika Praha +420246019719
Ireland Dublin +35316526556
Norge Oslo +4721031366
Finland Helsset +358942419041
Sverige Stockholm +46852503438
Ελλάς Αθήνα +302111768494
Magyarország Budapest +3619980547
GENTAUR Poland Sp. z o.o.
ul. Grunwaldzka 88/A m.2
81-771 Sopot, Poland
Tel 058 710 33 44
Fax 058 710 33 48
GENTAUR Nederland BV
5521 DG Eersel Nederland
Tel 0208-080893 Fax 0497-517897
Piazza Giacomo Matteotti, 6, 24122 Bergamo
Tel 02 36 00 65 93 Fax 02 36 00 65 94
53 Iskar Str. 1191 Kokalyane, Sofia