ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998
A Ca2+-independent receptor for alpha-latrotoxin, CIRL, mediates effects on secretion via multiple mechanisms.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 47 citations in OpenAlex.
- Adhesion G protein-coupled receptors.Pharmacological reviews · 2026Review
- Association of adaptor protein TRIP8b with clathrin.Journal of neurochemistry · 2011Article
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- G protein-coupled receptor expression in the adult and fetal adrenal glands.Molecular and cellular endocrinology · 2009Article
- Alpha-synuclein overexpression in PC12 and chromaffin cells impairs catecholamine release by interfering with a late step in exocytosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- alpha-Latrotoxin increases spontaneous and depolarization-evoked exocytosis from pancreatic islet beta-cells.The Journal of physiology · 2005Article
- The alpha-latrotoxin mutant LTXN4C enhances spontaneous and evoked transmitter release in CA3 pyramidal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- alpha-latrotoxin triggers transmitter release via direct insertion into the presynaptic plasma membrane.The EMBO journal · 2000Article
- Inhibition of quantal release from motor nerve by wortmannin.British journal of pharmacology · 1999Article
- alpha-Latrotoxin alters spontaneous and depolarization-evoked quantal release from rat adrenal chromaffin cells: evidence for multiple modes of action.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- Novel GPS-containing G protein-coupled receptor from Monosiga brevicollis.Doklady. Biochemistry and biophysicsArticle
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
alpha-Latrotoxin (alpha-Ltx), a component of black widow spider venom, stimulates secretion from nerve terminals and from PC12 cells. In this study we examine the effects of expression of a newly cloned Ca2+-independent receptor for alpha-Ltx (CIRL) on secretion from bovine chromaffin cells. We first characterized the effect of alpha-Ltx on secretion from untransfected cells. alpha-Ltx, by binding in a Ca2+-independent manner to an endogenous receptor, causes subsequent Ca2+-dependent secretion from intact cells. The stimulation of secretion is correlated with Ca2+ influx caused by the toxin. In permeabilized cells in which the Ca2+ concentration is regulated by buffer, alpha-Ltx also enhances Ca2+-dependent secretion, indicating a direct role of the endogenous receptor in the secretory pathway. Expression of CIRL increased the sensitivity of intact and permeabilized cells to the effects of alpha-Ltx, demonstrating that this protein is functional in coupling to secretion. Importantly, in the absence of alpha-Ltx, the expression of CIRL specifically inhibited the ATP-dependent component of secretion in permeabilized cells without affecting the ATP-independent secretion. This suggests that this receptor modulates the normal function of the regulated secretory pathway and that alpha-Ltx may act by reversing the inhibitory effects of the receptor.
Indexed as
Identifiers
9526008PMC6792605W2111037724What OpenQuestion holds
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.