Results 41 to 50 of about 582,708 (219)

Quantal responses to inositol 1,4,5-trisphosphate are not a consequence of Ca2+ regulation of inositol 1,4,5-trisphosphate receptors [PDF]

open access: yesBiochemical Journal, 1995
Submaximal concentrations of inositol 1,4,5-trisphosphate (InsP3) rapidly release only a fraction of the InsP3-sensitive intracellular Ca2+ stores, despite the ability of further increases in InsP3 concentration to evoke further Ca2+ release. The mechanisms underlying such quantal Ca2+ mobilization are not understood, but have been proposed to involve ...
S, Patel, C W, Taylor
openaire   +2 more sources

Junctate is a key element in calcium entry induced by activation of InsP3 receptors and/or calcium store depletion [PDF]

open access: yes, 2004
In many cell types agonist-receptor activation leads to a rapid and transient release of Ca(2+) from intracellular stores via activation of inositol 1,4,5 trisphosphate (InsP(3)) receptors (InsP(3)Rs).
Arnoult, Christophe   +38 more
core   +1 more source

Identification and characterization of insulin-like growth factor receptors on adult rat cardiac myocytes: linkage to inositol 1,4,5-trisphosphate formation. [PDF]

open access: yes, 1992
Cultured cardiac myocytes from adult Sprague-Dawley rats express both insulin-like growth factor-I (IGF-I) receptors and insulin-like growth factor-II/mannose 6-phosphate (IGF-II/Man6P) receptors and respond to IGF-I with a dose-dependent accumulation of
Berg, Ingeborg   +6 more
core   +2 more sources

Regulatory Mechanisms and Pathophysiological Significance of IP3 Receptors and Ryanodine Receptors in Drug Dependence

open access: yesJournal of Pharmacological Sciences, 2013
Calcium is a ubiquitous intracellular signaling molecule required for initiating and regulating neuronal functions. Ca2+ release from intracellular stores in the endoplasmic reticulum into intracellular spaces via intracellular Ca2+–releasing channels ...
Koji Mizuno   +2 more
doaj   +1 more source

Regulation of store-operated Ca2+ entry by IP3 receptors independent of their ability to release Ca2+

open access: yeseLife, 2023
Loss of endoplasmic reticular (ER) Ca2+ activates store-operated Ca2+ entry (SOCE) by causing the ER localized Ca2+ sensor STIM to unfurl domains that activate Orai channels in the plasma membrane at membrane contact sites (MCS).
Pragnya Chakraborty   +7 more
doaj   +1 more source

Endothelin-Induced Sarcoplasmic Reticulum Calcium Depletion Waves in Vascular Smooth Muscle Cells [PDF]

open access: yes, 2011
Agonist-stimulated waves of elevated cytoplasmic Ca2+ concentration ([Ca2+]i ) regulate blood vessel tone and vasomotion in vascular smooth muscle. Previous studies employing cytoplasmic Ca2+ indicators revealed that these Ca2+ waves were generated by a ...
Cornelis van Breemen   +7 more
core   +1 more source

Both neurons and astrocytes exhibited tetrodotoxin-resistant metabotropic glutamate receptor-dependent spontaneous slow Ca2+ oscillations in striatum.

open access: yesPLoS ONE, 2014
The striatum plays an important role in linking cortical activity to basal ganglia outputs. Group I metabotropic glutamate receptors (mGluRs) are densely expressed in the medium spiny projection neurons and may be a therapeutic target for Parkinson's ...
Atsushi Tamura   +5 more
doaj   +1 more source

The Inositol- 1,4,5=Trisphosphate System Is Involved in Rapid Effects of Aldosterone in Human Mononuclear Leukocytes [PDF]

open access: yes, 1993
There is increasing evidence for rapid steroid action on electrolyte transport in human mononuclear leukocytes (HML). In HML, aldosterone stimulates the Na+/H+ antiporter within a few minutes. Because a variety of hormones and growth factors activate the
Wehling, Martin   +5 more
core   +1 more source

Ca2+-Dependent Inositol 1,4,5-Trisphosphate and Nitric Oxide Signaling in Cerebellar Neurons

open access: yesJournal of Pharmacological Sciences, 2006
.: Intracellular Ca2+ signals are important for the regulation of synaptic functions in the central nervous system. In this review, I summarize findings of our recent studies on upstream and downstream Ca2+ signaling mechanisms in cerebellar synapses ...
Masamitsu Iino
doaj   +1 more source

Deranged calcium signaling and neurodegeneration in spinocerebellar ataxia type 3 [PDF]

open access: yes, 2008
Spinocerebellar ataxia type 3 (SCA3), also known as Machado-Joseph disease (MJD), is an autosomal-dominant neurodegenerative disorder caused by a polyglutamine expansion in ataxin-3 (SCA3, MJD1) protein.
X. Chen   +15 more
core   +1 more source

Home - About - Disclaimer - Privacy