ArticleThe Biochemical journal1999
Calexcitin interaction with neuronal ryanodine receptors.
Article in The Biochemical journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 36 citations in OpenAlex.
- Three muscle-specific DAF-16/FOXO transcriptional targets activated by reduced insulin/IGF-1 signaling.G3 (Bethesda, Md.) · 2026Article
- Binding of Gd(3+) to the neuronal signalling protein calexcitin identifies an exchangeable Ca(2+)-binding site.Acta crystallographica. Section F, Structural biology communications · 2016Article
- Genotype-phenotype correlations in recessive RYR1-related myopathies.Orphanet journal of rare diseases · 2013Article
- Crystallization and preliminary X-ray diffraction analysis of calexcitin from Loligo pealei: a neuronal protein implicated in learning and memory.Acta crystallographica. Section F, Structural biology and crystallization communications · 2005Article
- Distinct intracellular calcium transients in neurites and somata integrate neuronal signals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- Effects of dantrolene on steps of excitation-contraction coupling in mammalian skeletal muscle fibers.The Journal of general physiology · 2001Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calexcitin (CE), a Ca2+- and GTP-binding protein, which is phosphorylated during memory consolidation, is shown here to co-purify with ryanodine receptors (RyRs) and bind to RyRs in a calcium-dependent manner. Nanomolar concentrations of CE released up to 46% of the 45Ca label from microsomes preloaded with 45CaCl2. This release was Ca2+-dependent and was blocked by antibodies against the RyR or CE, by the RyR inhibitor dantrolene, and by a seven-amino-acid peptide fragment corresponding to positions 4689-4697 of the RyR, but not by heparin, an Ins(1,4,5)P3-receptor antagonist. Anti-CE antibodies, in the absence of added CE, also blocked Ca2+ release elicited by ryanodine, suggesting that the CE and ryanodine binding sites were in relative proximity. Calcium imaging with bis-fura-2 after loading CE into hippocampal CA1 pyramidal cells in hippocampal slices revealed slow, local calcium transients independent of membrane depolarization. Calexcitin also released Ca2+ from liposomes into which purified RyR had been incorporated, indicating that CE binding can be a proximate cause of Ca2+ release. These results indicated that CE bound to RyRs and suggest that CE may be an endogenous modulator of the neuronal RyR.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.