ArticleThe Biochemical journal2006
Reactivity of free thiol groups in type-I inositol trisphosphate receptors.
Article in The Biochemical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 41 citations in OpenAlex.
- Inositol 1,4,5-trisphosphate receptor - reactive oxygen signaling domain regulates excitation-contraction coupling in atrial myocytes.Journal of molecular and cellular cardiology · 2022Article
- Reactive Oxygen Species and Endothelial CaInternational journal of molecular sciences · 2021Review
- Redox regulation of type-I inositol trisphosphate receptors in intact mammalian cells.The Journal of biological chemistry · 2018Article
- Mercury promotes catecholamines which potentiate mercurial autoimmunity and vasodilation: implications for inositol 1,4,5-triphosphate 3-kinase C susceptibility in kawasaki syndrome.Korean circulation journal · 2013Review
- Protein S-glutathionylation enhances Ca2+-induced Ca2+ release via the IP3 receptor in cultured aortic endothelial cells.The Journal of physiology · 2012Article
- Calcium and reactive oxygen species in acute pancreatitis: friend or foe?Antioxidants & redox signaling · 2011Review
- Apoptosis and autophagy: decoding calcium signals that mediate life or death.Cold Spring Harbor perspectives in biology · 2010Review
- Calcium-dependent conformational changes in inositol trisphosphate receptors.The Journal of biological chemistry · 2010Article
- Redox-regulated heterogeneous thresholds for ligand recruitment among InsP3R Ca2+-release channels.Biophysical journal · 2010Article
- SR/ER-mitochondrial local communication: calcium and ROS.Biochimica et biophysica acta · 2009Review
- Rac1 modulates stimulus-evoked Ca(2+) release in neuronal growth cones via parallel effects on microtubule/endoplasmic reticulum dynamics and reactive oxygen species production.Molecular biology of the cell · 2009Article
- Mitochondria and metazoan epigenesis.Seminars in cell & developmental biology · 2009Review
- Surface accessibility and conformational changes in the N-terminal domain of type I inositol trisphosphate receptors: studies using cysteine substitution mutagenesis.The Journal of biological chemistry · 2009Article
- Inositol trisphosphate receptor Ca2+ release channels.Physiological reviews · 2007Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The IP3R (inositol 1,4,5-trisphosphate receptor) Ca2+-release channel is known to be sensitive to thiol redox state. The present study was undertaken to characterize the number and location of reactive thiol groups in the type-I IP3R. Using the fluorescent thiol-reactive compound monobromobimane we found that approx. 70% of the 60 cysteine residues in the type-I IP3R are maintained in the reduced state. The accessibility of these residues was assessed by covalently tagging the IP3R in membranes with a 5 kDa or 20 kDa MPEG [methoxypoly(ethylene glycol) maleimide]. MPEG reaction caused a shift in the mobility of IP3R on SDS/PAGE that was blocked by pretreatment of the membranes with dithiothreitol, N-ethylmaleimide, mersalyl or thimerosal, indicating that MPEG reactivity was specific to thiol groups on the IP3R. Trypsin cleavage of the type-I IP3R generates five defined domains. In cerebellum membranes, MPEG reacted over a 5 min interval with tryptic fragment I and fragment III, but not fragments II, IV or V. Fragment I appears as a doublet in cerebellum membranes, corresponding to the presence and absence of the SI splice site in this region (SI is a spliced domain corresponding to amino acids 318-332). Only the fragment I band corresponding to the SI(+) splice form shifted after reaction with MPEG. Expression of SI(+) and SI(-) spliced forms in COS cell microsomes confirmed this result. The MPEG-induced shift was not prevented when the cysteine residue present in the SI splice domain (C326A) or the remaining seven cysteine residues in fragment I were individually mutated. Of the combination mutations screened, only the mutation of C206/214/326A blocked MPEG reactivity in fragment I. We conclude that a set of highly reactive cysteine residues in fragment I are differentially accessible in the SI(+) and SI(-) splice variants of the type-I IP3R.
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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.