Results 21 to 30 of about 411,380 (346)

Neurotoxicity induced by bupivacaine via T-type calcium channels in SH-SY5Y cells. [PDF]

open access: yesPLoS ONE, 2013
There is concern regarding neurotoxicity induced by the use of local anesthetics. A previous study showed that an overload of intracellular calcium is involved in the neurotoxic effect of some anesthetics.
Xianjie Wen   +6 more
doaj   +1 more source

Verapamil Block of T-Type Calcium Channels [PDF]

open access: yesMolecular Pharmacology, 2011
Verapamil is a prototypical phenylalkylamine (PAA), and it was the first calcium channel blocker to be used clinically. It tonically blocks L-type channels in the inner pore with micromolar affinity, and its affinity increases at depolarized membrane potentials.
Pamela, Bergson   +4 more
openaire   +2 more sources

Electrophysiological characterization of a Cav3.2 calcium channel missense variant associated with epilepsy and hearing loss

open access: yesMolecular Brain, 2023
T-type calcium channelopathies encompass a group of human disorders either caused or exacerbated by mutations in the genes encoding different T-type calcium channels.
Robin N. Stringer   +4 more
doaj   +1 more source

L- and T-type calcium channels control aldosterone production from human adrenals.

open access: yesJournal of Endocrinology, 2020
Aldosterone, which plays a key role in the regulation of blood pressure, is produced by zona glomerulosa (ZG) cells of the adrenal cortex. Exaggerated overproduction of aldosterone from ZG cells causes primary hyperaldosteronism.
Tingting Yang   +4 more
semanticscholar   +1 more source

Genetic Deletion of KLHL1 Leads to Hyperexcitability in Hypothalamic POMC Neurons and Lack of Electrical Responses to Leptin

open access: yesFrontiers in Neuroscience, 2021
Kelch-like 1 (KLHL1) is a neuronal actin-binding protein that modulates voltage-gated calcium channels. The KLHL1 knockout (KO) model displays altered calcium channel expression in various brain regions.
Paula P. Perissinotti   +4 more
doaj   +1 more source

Contribution of T-Type Calcium Channels to Spinal Cord Injury-Induced Hyperexcitability of Nociceptors

open access: yesJournal of Neuroscience, 2020
A hyperexcitable state and spontaneous activity of nociceptors have been suggested to play a critical role in the development of chronic neuropathic pain following spinal cord injury (SCI).
Justas Lauzadis   +5 more
semanticscholar   +1 more source

Weft, Warp & Weave: The Intricate Tapestry of Calcium Channels Regulating T Lymphocyte Function

open access: yesFrontiers in Immunology, 2013
Calcium (Ca2+) is a universal second messenger important for T lymphocyte homeostasis, activation, proliferation, differentiation and apoptosis. The events surrounding Ca2+ mobilization in lymphocytes are tightly regulated and involve the coordination of
Kyla D Omilusik   +3 more
doaj   +1 more source

Interactions of short-term and chronic treadmill training with aging of the left ventricle of the heart [PDF]

open access: yes, 2015
With aging, there is a decline in cardiac function accompanying increasing risk of arrhythmias. These effects are likely to be mechanistically associated with age-associated changes in calcium regulation within cardiac myocytes.
Close, Graeme L.   +6 more
core   +2 more sources

Static Magnetic Fields Regulate T-Type Calcium Ion Channels and Mediate Mesenchymal Stem Cells Proliferation

open access: yesCells, 2022
The static magnetic fields (SMFs) impact on biological systems, induce a variety of biological responses, and have been applied to the clinical treatment of diseases. However, the underlying mechanisms remain largely unclear.
Haokaifeng Wu   +14 more
semanticscholar   +1 more source

Tweeters and Woofers: The Complex Orchestra of Calcium Currents in T Lymphocytes

open access: yesFrontiers in Immunology, 2015
Elevation of intracellular calcium ion (Ca2+) levels is a vital event that regulates T lymphocyte homeostasis, activation, proliferation, differentiation, and apoptosis.
Lilian L Nohara   +12 more
doaj   +1 more source

Home - About - Disclaimer - Privacy