ReviewThe Biochemical journal1999
Protein-protein interactions in intracellular Ca2+-release channel function.
Review 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 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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
56 citing papers in PubMed, 205 citations in OpenAlex.
- Identification of Protein-Protein Interaction Associated Functions Based on Gene Ontology.The protein journal · 2024Article
- Calcium and Neural Stem Cell Proliferation.International journal of molecular sciences · 2024Review
- Ryanodine receptor RyR1-mediated elevation of CaJournal of animal science and biotechnology · 2022Article
- Article
- Targeting Bcl-2-IPBiochimica et biophysica acta. Molecular cell research · 2018Review
- Sexual Dimorphism in a Reciprocal Interaction of Ryanodine and IPThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Effect of M-phase kinase phosphorylations on type 1 inositol 1,4,5-trisphosphate receptor-mediated Ca2+ responses in mouse eggs.Cell calcium · 2015Article
- CCDI: a new ligand that modulates mammalian type 1 ryanodine receptor (RyR1).British journal of pharmacology · 2014Article
- Patch-clamp electrophysiology of intracellular Ca2+ channels.Cold Spring Harbor protocols · 2013Article
- Role of nociceptor αCaMKII in transition from acute to chronic pain (hyperalgesic priming) in male and female rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Dust from hog confinement facilities impairs Ca2+ mobilization from sarco(endo)plasmic reticulum by inhibiting ryanodine receptors.Journal of applied physiology (Bethesda, Md. : 1985) · 2013Article
- Permeant calcium ion feed-through regulation of single inositol 1,4,5-trisphosphate receptor channel gating.The Journal of general physiology · 2012Article
- Cloning and characterization of a calcium binding EF-hand protein gene TaCab1 from wheat and its expression in response to Puccinia striiformis f. sp. tritici and abiotic stresses.Molecular biology reports · 2011Article
- Ca2+ signaling during mammalian fertilization: requirements, players, and adaptations.Cold Spring Harbor perspectives in biology · 2011Review
- STIM proteins and the endoplasmic reticulum-plasma membrane junctions.Annual review of biochemistry · 2011Review
- Two-pore channels: Regulation by NAADP and customized roles in triggering calcium signals.Cell calcium · 2010Review
- Identification and characterization of endonuclein binding proteins: evidence of modulatory effects on signal transduction and chaperone activity.BMC biochemistry · 2009Article
- Homer and the ryanodine receptor.European biophysics journal : EBJ · 2009Review
- Structural and functional link between the mitochondrial network and the endoplasmic reticulum.The international journal of biochemistry & cell biology · 2009Review
- In vitro modulation of the cardiac ryanodine receptor activity by Homer1.Pflugers Archiv : European journal of physiology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Release of Ca2+ ions from intracellular stores can occur via two classes of Ca2+-release channel (CRC) protein, the inositol 1,4, 5-trisphosphate receptors (InsP3Rs) and the ryanodine receptors (RyRs). Multiple isoforms and subtypes of each CRC class display distinct but overlapping distributions within mammalian tissues. InsP3Rs and RyRs interact with a plethora of accessory proteins which modulate the activity of their intrinsic channels. Although many aspects of CRC structure and function have been reviewed in recent years, the properties of proteins with which they interact has not been comprehensively surveyed, despite extensive current research on the roles of these modulators. The aim of this article is to review the regulation of CRC activity by accessory proteins and, wherever possible, to outline the structural details of such interactions. The CRCs are large transmembrane proteins, with the bulk of their structure located cytoplasmically. Intra- and inter-complex protein-protein interactions between these cytoplasmic domains also regulate CRC function. Some accessory proteins modulate channel activity of all CRC subtypes characterized, whereas other have class- or even isoform-specific effects. Certain accessory proteins exert both direct and indirect forms of regulation on CRCs, occasionally with opposing effects. Others are themselves modulated by changes in Ca2+ concentration, thereby participating in feedback mechanisms acting on InsP3R and RyR activity. CRCs are therefore capable of integrating numerous signalling events within a cell by virtue of such protein-protein interactions. Consequently, the functional properties of InsP3Rs and RyRs within particular cells and subcellular domains are 'customized' by the accessory proteins present.
Indexed as
Identifiers
9895277PMC1219985W2150396353What 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.