scholarly journals Molecular cloning in yeast by in vivo homologous recombination of the yeast putative α1 subunit of the voltage-gated calcium channel

FEBS Letters ◽  
2004 ◽  
Vol 576 (3) ◽  
pp. 291-296 ◽  
Author(s):  
Kazuko Iida ◽  
Tomoko Tada ◽  
Hidetoshi Iida
Keyword(s):  
Homologous Recombination ◽  
Calcium Channel ◽  
Molecular Cloning ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channel ◽  
Α1 Subunit

Alterations in hippocampal voltage-gated calcium channel α1 subunit expression patterns after kainate-induced status epilepticus in aging rats

2003 ◽  
Vol 57 (1) ◽  
pp. 15-32 ◽  
Author(s):  
Kevin M. Kelly ◽  
Milos D. Ikonomovic ◽  
Eric E. Abrahamson ◽  
Elena A. Kharlamov ◽  
Teresa M. Hentosz ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Calcium Channel ◽  
Expression Patterns ◽  
Aging Rats ◽  
Voltage Gated ◽  
Subunit Expression ◽  
Voltage Gated Calcium Channel ◽  
Α1 Subunit

Molecular Cloning and Characterization of the Human Voltage-Gated Calcium Channel α2δ-4 Subunit

2002 ◽  
Vol 62 (3) ◽  
pp. 485-496 ◽  
Author(s):  
Ning Qin ◽  
Susan Yagel ◽  
Mary-Lou Momplaisir ◽  
Ellen E. Codd ◽  
Michael R. D'Andrea
Keyword(s):  
Calcium Channel ◽  
Molecular Cloning ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channel

scholarly journals straightjacket is required for the synaptic stabilization of cacophony, a voltage-gated calcium channel α1 subunit

2008 ◽  
Vol 181 (1) ◽  
pp. 157-170 ◽  
Author(s):  
Cindy V. Ly ◽  
Chi-Kuang Yao ◽  
Patrik Verstreken ◽  
Tomoko Ohyama ◽  
Hugo J. Bellen
Keyword(s):  
Calcium Channel ◽  
Neuronal Excitability ◽  
Neuromuscular Junctions ◽  
Synaptic Function ◽  
Voltage Gated ◽  
Α2δ Subunit ◽  
Voltage Gated Calcium Channel ◽  
Α1 Subunit ◽  
Synaptic Level ◽  
Synaptic Stabilization

In a screen to identify genes involved in synaptic function, we isolated mutations in Drosophila melanogaster straightjacket (stj), an α2δ subunit of the voltage-gated calcium channel. stj mutant photoreceptors develop normal synaptic connections but display reduced “on–off” transients in electroretinogram recordings, indicating a failure to evoke postsynaptic responses and, thus, a defect in neurotransmission. stj is expressed in neurons but excluded from glia. Mutants exhibit endogenous seizure-like activity, indicating altered neuronal excitability. However, at the synaptic level, stj larval neuromuscular junctions exhibit approximately fourfold reduction in synaptic release compared with controls stemming from a reduced release probability at these synapses. These defects likely stem from destabilization of Cacophony (Cac), the primary presynaptic α1 subunit in D. melanogaster. Interestingly, neuronal overexpression of cac partially rescues the viability and physiological defects in stj mutants, indicating a role for the α2δ Ca2+ channel subunit in mediating the proper localization of an α1 subunit at synapses.

Comparative genomics of the human and Fugu voltage-gated calcium channel α1-subunit gene family reveals greater diversity in Fugu

Gene ◽  
2006 ◽  
Vol 366 (1) ◽  
pp. 117-127 ◽  
Author(s):  
Esther Wong ◽  
Wei-Ping Yu ◽  
Wai Ho Yap ◽  
Byrappa Venkatesh ◽  
Tuck Wah Soong
Keyword(s):  
Comparative Genomics ◽  
Calcium Channel ◽  
Gene Family ◽  
Subunit Gene ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channel ◽  
Α1 Subunit

Abstract 15494: Physiological Investigation of the C57bl6 Mouse Aorta Reveals a Critical Role for Voltage Gated Calcium Channel Activity in Spontaneous Arterial Ageing

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Sofie De Moudt ◽  
Jhana O Hendrickx ◽  
Dorien G De Munck ◽  
Arthur J Leloup ◽  
Wim Martinet ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Ex Vivo ◽  
Arterial Compliance ◽  
Critical Role ◽  
Aortic Pulse Wave Velocity ◽  
Physiological Ageing ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channel ◽  
Set Up

Introduction: Arterial stiffness (AS) has gained much recognition as a hallmark and independent predictor of cardiovascular (CV) events. Although generally assumed to be an adaptive response to increased blood pressure (BP), AS precedes hypertension in at least two experimental mouse models, thus revealing an incomplete understanding of AS pathophysiology. Methods: The current study presents the longitudinal CV characterization of spontaneously ageing C57Bl6 mice (2, 4, 6, 9, 12 and 24-month old) (male, n>8). In vivo analysis of peripheral BP (Coda), aortic pulse wave velocity (aPWV, Vevo2100), and echocardiography (Vevo2100) was combined with ex vivo aortic studies of isometric reactivity (organ baths) and AS measurements in the Rodent Oscillatory Tension set-up for Arterial Compliance (ROTSAC). (Data are presented as mean ± SEM.) Results: In vivo and ex vivo characterisation confirms that aortic stiffness precedes peripheral BP alterations in spontaneously ageing C57Bl6 mice, with significantly and gradually increasing aPWV (Fig.A) and isobaric Peterson modulus (Ep) (Fig.B) from 6-month of age onward. Thereafter, cardiac hypertrophy was observed at 9-months of age (Fig.C), and peripheral BP measurement reveals elevated pulse pressure at 24-months (30% increase vs. all other ages) (Fig.D). Ex vivo investigation of the thoracic aorta shows increased contractions to phenylephrine (PE) in old (6-24 month) vs. young (2-4 month) mice (Fig.E,F) with an increased contribution of voltage-gated calcium channel (VGCC) (Fig.G,H) with age. Remarkably, no differences were observed on endothelial function, meaning that all changes occur on the level of the vascular smooth muscle cell (VSMC). Conclusions: Physiological ageing of VSMC results in high PE contractions, increased VGCC activity, and the development of significant arterial stiffening by 6-months of age. AS thereby precedes the development of peripheral BP alterations by 18 months.

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