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ZD7288 inhibits low-threshold Ca(2+) channel activity and regulates sperm function.
Rim1 modulates direct G-protein regulation of Cav2.2 channels
The data suggest that Rim1-induced facilitation of neurotransmitter release may come as a consequence of a decrease in the inhibitory pathway carried by G-proteins that contributes, together with the slowing of channel inactivation, to maintain Ca2+ influx under prolonged activity.
Intramembrane Charge Movement Associated with Endogenous K+ Channel Activity in HEK-293 Cells
Gating currents were unambiguously resolved after ionic current blockade enabling this first report of intramembrane charge movement in HEK-293 cells arising entirely from endogenous K+ channel activity, and providing valuable information concerning the activation mechanism of voltage-gated K+ channels in these cells.
The S218L familial hemiplegic migraine mutation promotes deinhibition of Cav2.1 calcium channels during direct G-protein regulation
Functional consequences of FHM-1 mutations appear as the consequence of the alteration of both intrinsic biophysical properties and of the main inhibitory G-protein pathway of Cav2.1 channels, which seems in line with the less severe associated clinical phenotype in patients.
Adenosine Stimulate Proliferation and Migration in Triple Negative Breast Cancer Cells
It is shown that Ado increases proliferation and migration in a triple negative breast cancer model, the MDA-MB 231 cell line, which suggests important roles of the A2B receptors and NaV1.5 channels in the Ado-induced increase in proliferation and migrated cells.
Cdk5-Dependent Phosphorylation of CaV3.2 T-Type Channels: Possible Role in Nerve Ligation-Induced Neuropathic Allodynia and the Compound Action Potential in Primary Afferent C Fibers
The present work shows that the exacerbated expression of Cdk5 in a preclinical model of neuropathic pain increases the functional expression of CaV3.2 channels, and suggests that increased channel activity by Cdk 5-mediated phosphorylation after SNL contributes nerve injury-induced tactile allodynia.