ArticleNeuroscience and behavioral physiology
Low-conductivity calcium channels in the macrophage plasma membrane: activation by inositol-1,4,5-triphosphate.
Article in Neuroscience and behavioral physiology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 12 citations in OpenAlex.
- The transcription factor nuclear factor of activated T cells c3 modulates the function of macrophages in sepsis.Journal of innate immunity · 2014Article
- Activation of the inositol (1,4,5)-triphosphate calcium gate receptor is required for HIV-1 Gag release.Journal of virology · 2010Article
- ORAI1 and STIM1 deficiency in human and mice: roles of store-operated Ca2+ entry in the immune system and beyond.Immunological reviews · 2009Review
- Close functional coupling between Ca2+ release-activated Ca2+ channels and reactive oxygen species production in murine macrophages.Mediators of inflammation · 2006Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Local voltage clamping was applied to mouse macrophage plasma membrane to study calcium channels activated by inositol-1,4,5-triphosphate (IP3) and blocked by heparin. These channels were clearly distinguished from IP3-activated channels of the endoplasmic reticulum by their low conductivity (about 1 pSm for 100 mM Ca2+), high selectivity for Ca2+ relative to K+ (P(Ca):P(K) > 1000), calcium inactivation, and activation on hyperpolarization; these properties allowed them to be assigned to the I(CRAC) family. On the other hand, the properties of the IP3 receptors of these channels (IP3R), i.e., the dose-dependent effect of IP3, the IP3 desensitization of the receptor, and the sensitivity to micromolar concentrations of heparin and arachidonic acid were close to those of the endoplasmic reticulum IP3 receptor. The most likely interpretation of these data is that IP3R are not located in the endoplasmic reticulum, but, acting via some kind of conformational change occurring on binding of IP3, transmit a signal from the endoplasmic reticulum to the highly selective Ca2+ channels. This point of view is in agreement with the published "coupling model" [1].
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