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https://www.readbyqxmd.com/read/27913207/overexpression-of-stim1-in-neurons-in-mouse-brain-improves-contextual-learning-and-impairs-long-term-depression
#1
Łukasz Majewski, Filip Maciąg, Paweł M Boguszewski, Iga Wasilewska, Grzegorz Wiera, Tomasz Wójtowicz, Jerzy Mozrzymas, Jacek Kuznicki
STIM1 is an endoplasmic reticulum calcium sensor that is involved in several processes in neurons, including store-operated calcium entry. STIM1 also inhibits voltage-gated calcium channels, such as Cav1.2 and Cav3.1, and is thus considered a multifunctional protein. The aim of this work was to investigate the ways in which transgenic neuronal overexpression of STIM1 in FVB/NJ mice affects animal behavior and the electrophysiological properties of neurons in acute hippocampal slices. We overexpressed STIM1 from the Thy1...
November 29, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27906063/characterization-of-a-multiprotein-complex-involved-in-excitation-transcription-coupling-of-skeletal-muscle
#2
Manuel Arias-Calderón, Gonzalo Almarza, Alexis Díaz-Vegas, Ariel Contreras-Ferrat, Denisse Valladares, Mariana Casas, Héctor Toledo, Enrique Jaimovich, Sonja Buvinic
BACKGROUND: Electrical activity regulates the expression of skeletal muscle genes by a process known as "excitation-transcription" (E-T) coupling. We have demonstrated that release of adenosine 5'-triphosphate (ATP) during depolarization activates membrane P2X/P2Y receptors, being the fundamental mediators between electrical stimulation, slow intracellular calcium transients, and gene expression. We propose that this signaling pathway would require the proper coordination between the voltage sensor (dihydropyridine receptor, DHPR), pannexin 1 channels (Panx1, ATP release conduit), nucleotide receptors, and other signaling molecules...
April 11, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27902567/dorsal-root-ganglion-neurons-become-hyperexcitable-and-increase-expression-of-voltage-gated-t-type-calcium-channels-cav3-2-in-paclitaxel-induced-peripheral-neuropathy
#3
Yan Li, Claudio Esteves Tatsui, Laurence D Rhines, Robert Y North, Daniel S Harrison, Ryan M Cassidy, Caj A Johansson, Alyssa K Kosturakis, Denaya D Edwards, Hongmei Zhang, Patrick M Dougherty
Here it is shown that paclitaxel induced neuropathy is associated with the development of spontaneous activity (SA) and hyperexcitability in DRG neurons that is paralleled by increased expression of low-voltage-activated calcium channels (T-type; Cav3.2). The percentage of DRG neurons showing SA and the overall mean rate of SA were significantly higher at day 7 of paclitaxel treatment than in rats receiving vehicle. Cav3.2 expression was increased in L4-6 DRG and spinal cord segments in paclitaxel-treated rats, localized to small calcitonin gene-related peptide expressing and isolectin B4 expressing DRG neurons and to glial fibrillary acidic protein-positive spinal cord cells...
November 24, 2016: Pain
https://www.readbyqxmd.com/read/27882143/expression-of-connexin-43-ion-channels-and-ca-2-handling-proteins-in-rat-pulmonary-vein-cardiomyocytes
#4
Yaqiong Xiao, Xue Cai, Andrew Atkinson, Sunil Jit Logantha, Mark Boyett, Halina Dobrzynski
Atrial fibrillation (AF) is the most common cardiac arrhythmia. AF is thought to be triggered by ectopic beats, originating primarily in the myocardial sleeves surrounding the pulmonary veins (PVs). The mechanisms underlying these cardiac arrhythmias remain unclear. To investigate this, frozen sections of heart and lung tissue from adult rats without arrhythmia were obtained in different planes, stained with Masson's trichrome, and immunolabeled for connexin 43 (Cx43), caveolin-3 (Cav3), hyperpolarization-activated cyclic nucleotide-gated channel 4 (HCN4), Nav1...
November 2016: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/27843503/review-cav2-3-r-type-voltage-gated-ca-2-channels-functional-implications-in-convulsive-and-non-convulsive-seizure-activity
#5
Carola Wormuth, Andreas Lundt, Christina Henseler, Ralf Müller, Karl Broich, Anna Papazoglou, Marco Weiergräber
BACKGROUND: Researchers have gained substantial insight into mechanisms of synaptic transmission, hyperexcitability, excitotoxicity and neurodegeneration within the last decades. Voltage-gated Ca(2+) channels are of central relevance in these processes. In particular, they are key elements in the etiopathogenesis of numerous seizure types and epilepsies. Earlier studies predominantly targeted on Cav2.1 P/Q-type and Cav3.2 T-type Ca(2+) channels relevant for absence epileptogenesis. Recent findings bring other channels entities more into focus such as the Cav2...
2016: Open Neurology Journal
https://www.readbyqxmd.com/read/27772553/cav3-mutation-in-a-patient-with-transient-hyperckemia-and-myalgia
#6
Anna Macias, Tomasz Gambin, Przemyslaw Szafranski, Shalini N Jhangiani, Anna Kolasa, Ewa Obersztyn, James R Lupski, Pawel Stankiewicz, Anna Kaminska
Mutations in caveolin-3 (CAV3) can lead to different clinical phenotypes affecting skeletal or cardiac muscles. Here, we describe a patient with Klinefelter syndrome, ulcerative colitis and Sjögren syndrome, who developed transient hyperCKemia, myalgia and mild muscular weakness. Using whole exome sequencing (WES), a missense mutation G169A was found in the CAV3 gene. In addition, we identified a homozygous frameshift deletion in MS4A12 that may contribute to inflammatory bowel disease, further demonstrating usefulness of WES in dual molecular diagnoses...
November 2016: Neurologia i Neurochirurgia Polska
https://www.readbyqxmd.com/read/27765616/chronic-intrathecal-infusion-of-t-type-calcium-channel-blockers-attenuates-cav3-2-upregulation-in-nerve-ligated-rats
#7
Sheng-Jie Shiue, Chi-Hsu Wang, Tao-Yeuan Wang, Yi-Chun Chen, Jen-Kun Cheng
OBJECTIVE: T-type channel (TCC) CaV3.2 plays a pivotal role in pain transmission. In this study, we examined the effects of intrathecal TCC blockers on CaV3.2 expression in a L5/6 spinal nerve ligation (SNL) pain model. The neurotoxicity of TCC blockers were also evaluated. METHODS: Male Sprague-Dawley rats (200-250 g) were used for right L5/6 SNL to induce neuropathic pain. Intrathecal infusion of saline or TCC blockers [mibefradil (0.7 μg/h) or ethosuximide (60 μg/h)] was started after surgery for 7 days...
October 17, 2016: Acta Anaesthesiologica Taiwanica: Official Journal of the Taiwan Society of Anesthesiologists
https://www.readbyqxmd.com/read/27756899/a-rare-schizophrenia-risk-variant-of-cacna1i-disrupts-cav3-3-channel-activity
#8
A Andrade, J Hope, A Allen, V Yorgan, D Lipscombe, J Q Pan
CACNA1I is a candidate schizophrenia risk gene. It encodes the pore-forming human CaV3.3 α1 subunit, a subtype of voltage-gated calcium channel that contributes to T-type currents. Recently, two de novo missense variations, T797M and R1346H, of hCaV3.3 were identified in individuals with schizophrenia. Here we show that R1346H, but not T797M, is associated with lower hCaV3.3 protein levels, reduced glycosylation, and lower membrane surface levels of hCaV3.3 when expressed in human cell lines compared to wild-type...
October 19, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27742704/na-k-cl-cotransporter-nkcc-maintains-the-chloride-gradient-to-sustain-pacemaker-activity-in-interstitial-cells-of-cajal
#9
Mei Hong Zhu, Tae Sik Sung, Masaaki Kurahashi, Lauren E O'Kane, Kate O'Driscoll, Sang Don Koh, Kenton M Sanders
Interstitial cells of Cajal (ICC) generate electrical slow waves by coordinated openings of ANO1 channels, a Ca(2+)-activated Cl(-) (CaCC) conductance. Efflux of Cl(-) during slow waves must be significant, as there is high current density during slow-wave currents and slow waves are of sufficient magnitude to depolarize the syncytium of smooth muscle cells and PDGFRα(+) cells to which they are electrically coupled. We investigated how the driving force for Cl(-) current is maintained in ICC. We found robust expression of Slc12a2 (which encodes an Na(+)-K(+)-Cl(-) cotransporter, NKCC1) and immunohistochemical confirmation that NKCC1 is expressed in ICC...
December 1, 2016: American Journal of Physiology. Gastrointestinal and Liver Physiology
https://www.readbyqxmd.com/read/27729216/cacna1h-mutations-are-associated-with-different-forms-of-primary-aldosteronism
#10
Georgios Daniil, Fabio L Fernandes-Rosa, Jean Chemin, Iulia Blesneac, Jacques Beltrand, Michel Polak, Xavier Jeunemaitre, Sheerazed Boulkroun, Laurence Amar, Tim M Strom, Philippe Lory, Maria-Christina Zennaro
Primary aldosteronism (PA) is the most common form of secondary hypertension. Mutations in KCNJ5, ATP1A1, ATP2B3 and CACNA1D are found in aldosterone producing adenoma (APA) and familial hyperaldosteronism (FH). A recurrent mutation in CACNA1H (coding for Cav3.2) was identified in a familial form of early onset PA. Here we performed whole exome sequencing (WES) in patients with different types of PA to identify new susceptibility genes. Four different heterozygous germline CACNA1H variants were identified. A de novo Cav3...
October 4, 2016: EBioMedicine
https://www.readbyqxmd.com/read/27718503/immunohistochemical-analysis-of-t-type-calcium-channels-in-acquired-melanocytic-nevi-and-melanoma
#11
O Maiques, A Macià, S Moreno, C Barceló, M Santacana, A Vea, J Herreros, S Gatius, E Ortega, J Valls, B J Chen, D Llobet-Navas, X Matias-Guiu, C Cantí, R M Marti
BACKGROUND AND OBJECTIVES: Cutaneous malignant melanoma arises from transformed melanocytes de novo or from congenital or acquired melanocytic nevi. We have recently reported that T-type Ca(2+) channels (TTCs) are upregulated in human melanoma and play an important role on cell proliferation. The aim of this study was to describe for the first time in formalin-fixed-paraffin-embedded tissue the immunoexpression of TT-Cs in biopsies of normal skin, acquired melanocytic nevi and melanoma, in order to evaluate their role in melanomagenesis and/or tumor progression, their utility as prognostic markers and their possible use in targeted therapies...
October 8, 2016: British Journal of Dermatology
https://www.readbyqxmd.com/read/27682595/stacking-up-cav3-2-channels
#12
Mircea C Iftinca, Christophe Altier
No abstract text is available yet for this article.
September 28, 2016: Channels
https://www.readbyqxmd.com/read/27659162/cooperative-roles-of-glucose-and-asparagine-linked-glycosylation-in-t-type-calcium-channel-expression
#13
Joanna Lazniewska, Yuriy Rzhepetskyy, Fang-Xiong Zhang, Gerald W Zamponi, Norbert Weiss
T-type calcium channels are key contributors to neuronal physiology where they shape electrical activity of nerve cells and contribute to the release of neurotransmitters. Enhanced T-type channel expression has been causally linked to a number of pathological conditions including peripheral painful diabetic neuropathy. Recently, it was demonstrated that asparagine-linked glycosylation not only plays an essential role in regulating cell surface expression of Cav3.2 channels, but may also support glucose-dependent potentiation of T-type currents...
September 23, 2016: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/27641070/inhibition-promotes-long-term-potentiation-at-cerebellar-excitatory-synapses
#14
F Binda, K Dorgans, S Reibel, K Sakimura, M Kano, B Poulain, P Isope
The ability of the cerebellar cortex to learn from experience ensures the accuracy of movements and reflex adaptation, processes which require long-term plasticity at granule cell (GC) to Purkinje neuron (PN) excitatory synapses. PNs also receive GABAergic inhibitory inputs via GCs activation of interneurons; despite the involvement of inhibition in motor learning, its role in long-term plasticity is poorly characterized. Here we reveal a functional coupling between ionotropic GABAA receptors and low threshold CaV3 calcium channels in PNs that sustains calcium influx and promotes long-term potentiation (LTP) at GC to PN synapses...
2016: Scientific Reports
https://www.readbyqxmd.com/read/27617699/tetrodotoxin-sensitive-ca2-currents-but-no-t-type-currents-in-normal-hypertrophied-and-failing-mouse-cardiomyocytes
#15
Ilona Bodi, Hiroyuki Nakayama, Arnold Schwartz
AIMS: To obtain functional evidence that ICa,T is involved in the pathogenesis of cardiac hypertrophy and heart failure. We unexpectedly identified ICa(TTX) rather than ICa,T, therefore, we adjusted our aim to encompass these findings. METHODS AND RESULTS: We investigated 1) Cav3.1 (α1G) transgenic (Tg) mice compared with non-transgenic (tTA-Ntg) 2) Cav3.1 deficient mice (Cav3.1) compared with wild-type (Wt) after chemically and surgically induced cardiac remodeling 3) Spontaneous hypertensive rats (SHR) and thoracic aorta constricting (TAC) rats...
September 7, 2016: Journal of Cardiovascular Pharmacology
https://www.readbyqxmd.com/read/27616982/ontogenic-changes-and-differential-localization-of-t-type-ca-2-channel-subunits-cav3-1-and-cav3-2-in-mouse-hippocampus-and-cerebellum
#16
Carolina Aguado, Sebastián García-Madrona, Mercedes Gil-Minguez, Rafael Luján
T-type calcium (Ca(2+)) channels play a central role in regulating membrane excitability in the brain. Although the contributions of T-type current to neuron output is often proposed to reflect a differential distribution of T-type channel subtypes to somato-dendritic compartments, their precise subcellular distributions in central neurons are not fully determined. Using histoblot and high-resolution immunoelectron microscopic techniques, we have investigated the expression, regional distribution and subcellular localization of T-type Cav3...
2016: Frontiers in Neuroanatomy
https://www.readbyqxmd.com/read/27612189/ptrf-cavin-1-deficiency-causes-cardiac-dysfunction-accompanied-by-cardiomyocyte-hypertrophy-and-cardiac-fibrosis
#17
Takuya Taniguchi, Naoki Maruyama, Takehiro Ogata, Takeru Kasahara, Naohiko Nakanishi, Kotaro Miyagawa, Daisuke Naito, Tetsuro Hamaoka, Masahiro Nishi, Satoaki Matoba, Tomomi Ueyama
Mutations in the PTRF/Cavin-1 gene cause congenital generalized lipodystrophy type 4 (CGL4) associated with myopathy. Additionally, long-QT syndrome and fatal cardiac arrhythmia are observed in patients with CGL4 who have homozygous PTRF/Cavin-1 mutations. PTRF/Cavin-1 deficiency shows reductions of caveolae and caveolin-3 (Cav3) protein expression in skeletal muscle, and Cav3 deficiency in the heart causes cardiac hypertrophy with loss of caveolae. However, it remains unknown how loss of PTRF/Cavin-1 affects cardiac morphology and function...
2016: PloS One
https://www.readbyqxmd.com/read/27571431/expression-patterns-of-t-type-cav3-2-channel-and-insulin-like-growth-factor-1-receptor-in-dorsal-root-ganglion-neurons-of-mice-after-sciatic-nerve-axotomy
#18
Si-Fang Lin, Xiao-Lu Yu, Xiao-Ya Liu, Bing Wang, Cheng-Hui Li, Yan-Gang Sun, Xing-Jun Liu
Substantial evidence indicates that T-type Cav3.2 channel and insulin-like growth factor-1 (IGF-1) contribute to pain hypersensitivity within primary sensory nerves. A recent study suggested that activation of IGF-1 receptor (IGF-1R) could increase Cav3.2 channel currents and further contribute to inflammatory pain sensitivity. However, the expression patterns of Cav3.2 and IGF-1R and their colocalization in dorsal root ganglion (DRG) in chronic neuropathic pain condition remain unknown. In this study, we explored expression patterns of Cav3...
October 19, 2016: Neuroreport
https://www.readbyqxmd.com/read/27508685/-op-lb01-12-cacna1h-mutations-are-associated-with-young-onset-and-familial-forms-of-primary-aldosteronism
#19
G Daniil, F L Fernandes-Rosa, J Chemin, X Jeunemaitre, M Polak, S Boulkroun, L Amar, T M Strom, P Lory, M C Zennaro
OBJECTIVE: Primary aldosteronism (PA) is the most common form of secondary hypertension. Mutations in KCNJ5, ATP1A1, ATP2B3 and CACNA1D are found in aldosterone producing adenomas (APA) and familial hyperaldosteronism (FH). Recently, a recurrent germline mutation in CACNA1H (encoding the T-type voltage-dependent calcium channel Cav3.2) was identified in a new familial form of early onset hypertension and PA. DESIGN AND METHOD: To identify new genes responsible for PA, we have performed whole exome sequencing in 23 patients with APA, 10 patients with FH and in two trios with the proband presenting early onset PA...
September 2016: Journal of Hypertension
https://www.readbyqxmd.com/read/27452469/%C3%AE-arrestin-dependent-dopaminergic-regulation-of-calcium-channel-activity-in-the-axon-initial-segment
#20
Sungchil Yang, Roy Ben-Shalom, Misol Ahn, Alayna T Liptak, Richard M van Rijn, Jennifer L Whistler, Kevin J Bender
G-protein-coupled receptors (GPCRs) initiate a variety of signaling cascades, depending on effector coupling. β-arrestins, which were initially characterized by their ability to "arrest" GPCR signaling by uncoupling receptor and G protein, have recently emerged as important signaling effectors for GPCRs. β-arrestins engage signaling pathways that are distinct from those mediated by G protein. As such, arrestin-dependent signaling can play a unique role in regulating cell function, but whether neuromodulatory GPCRs utilize β-arrestin-dependent signaling to regulate neuronal excitability remains unclear...
August 9, 2016: Cell Reports
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