ReviewMolecular neurobiology1996
Role of Drosophila TRP in inositide-mediated Ca2+ entry.
Review in Molecular neurobiology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 21 citations in OpenAlex.
- Upregulation and Diverse Roles of TRPC3 and TRPC6 in Synaptic Reorganization of the Mossy Fiber Pathway in Temporal Lobe Epilepsy.Molecular neurobiology · 2015Article
- The tyrosine kinase inhibitor bafetinib inhibits PAR2-induced activation of TRPV4 channels in vitro and pain in vivo.British journal of pharmacology · 2014Article
- Specific association of the gene product of PKD2 with the TRPC1 channel.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Effects of ethanol on calcium homeostasis in the nervous system: implications for astrocytes.Molecular neurobiology · 1999Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inositol lipid signaling relies on an InsP3-induced Ca2+ release from intracellular stores and on extracellular Ca2+ entry, which takes place when the Ca2+ stores become depleted of Ca2+. This interplay between Ca2+ release and Ca2+ entry has been termed capacitative Ca2+ entry and the inward current calcium release activated current (CRAC) to indicate gating of Ca2+ entry by Ca2+-store depletion. The signaling pathway and the gating mechanism of capacitative Ca2+ entry, however, are largely unknown and the molecular participants in this process have not been identified. In this article we review genetic, molecular, and functional studies of wild-type and mutant Drosophila photoreceptors, suggesting that the transient receptor potential mutant (trp) is the first putative capacitative Ca2+ entry mutant. Furthermore, several lines of evidence suggest that the trp gene product TRP is a candidate subunit of the plasma membrane channel that is activated by Ca2+ store depletion.
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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.