ArticleBiochemical and biophysical research communications2010
Stimulation of TRPC5 cationic channels by low micromolar concentrations of lead ions (Pb2+).
Article in Biochemical and biophysical research communications, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Lead Acetate Exposure and Cerebral Amyloid Accumulation: Mechanistic Evaluations in APP/PS1 Mice.Environmental health perspectives · 2024Article
- MOLECULAR MECHANISMS OF LEAD NEUROTOXICITY.Advances in neurotoxicology · 2021Article
- Englerin A-sensing charged residues for transient receptor potential canonical 5 channel activation.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2019Article
- Lead poisoning: acute exposure of the heart to lead ions promotes changes in cardiac function and Cav1.2 ion channels.Biophysical reviews · 2017Review
- Picomolar, selective, and subtype-specific small-molecule inhibition of TRPC1/4/5 channels.The Journal of biological chemistry · 2017Article
- Molecular Determinants of the Sensitivity to Gq/11-Phospholipase C-dependent Gating, Gd3+ Potentiation, and Ca2+ Permeability in the Transient Receptor Potential Canonical Type 5 (TRPC5) Channel.The Journal of biological chemistry · 2017Article
- Heavy metal chelator TPEN attenuates fura-2 fluorescence changes induced by cadmium, mercury and methylmercury.The Journal of veterinary medical science · 2016Article
- Defining potential roles of Pb(2+) in neurotoxicity from a calciomics approach.Metallomics : integrated biometal science · 2016Review
- Copper-Induced Membrane Depolarizations Involve the Induction of Mosaic TRP Channels, Which Activate VDCC Leading to Calcium Increases in Ulva compressa.Frontiers in plant science · 2016Article
- Permeation, regulation and control of expression of TRP channels by trace metal ions.Pflugers Archiv : European journal of physiology · 2015Review
- Copper-induced activation of TRP channels promotes extracellular calcium entry, activation of CaMs and CDPKs, copper entry and membrane depolarization in Ulva compressa.Frontiers in plant science · 2015Article
- Riluzole activates TRPC5 channels independently of PLC activity.British journal of pharmacology · 2014Article
- Rapid and contrasting effects of rosiglitazone on transient receptor potential TRPM3 and TRPC5 channels.Molecular pharmacology · 2011Article
- Properties and therapeutic potential of transient receptor potential channels with putative roles in adversity: focus on TRPC5, TRPM2 and TRPA1.Current drug targets · 2011Review
- Stereo-selective inhibition of transient receptor potential TRPC5 cation channels by neuroactive steroids.British journal of pharmacology · 2011Article
- TRPC5 channel sensitivities to antioxidants and hydroxylated stilbenes.The Journal of biological chemistry · 2011Article
- The roles of G proteins in the activation of TRPC4 and TRPC5 transient receptor potential channels.Channels (Austin, Tex.)Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Lead toxicity is long-recognised but continues to be a major public health problem. Its effects are wide-ranging and include induction of hyper-anxiety states. In general it is thought to act by interfering with Ca(2+) signalling but specific targets are not clearly identified. Transient receptor potential canonical 5 (TRPC5) is a Ca(2+)-permeable ion channel that is linked positively to innate fear responses and unusual amongst ion channels in being stimulated by trivalent lanthanides, which include gadolinium. Here we show investigation of the effect of lead, which is a divalent ion (Pb(2+)). Intracellular Ca(2+) and whole-cell patch-clamp recordings were performed on HEK 293 cells conditionally over-expressing TRPC5 or other TRP channels. Extracellular application of Pb(2+) stimulated TRPC5 at concentrations greater than 1 microM. Control cells without TRPC5 showed little or no response to Pb(2+) and expression of other TRP channels (TRPM2 or TRPM3) revealed partial inhibition by 10 microM Pb(2+). The stimulatory effect on TRPC5 depended on an extracellular residue (E543) near the ion pore: similar to gadolinium action, E543Q TRPC5 was resistant to Pb(2+) but showed normal stimulation by the receptor agonist sphingosine-1-phosphate. The study shows that Pb(2+) is a relatively potent stimulator of the TRPC5 channel, generating the hypothesis that a function of the channel is to sense metal ion poisoning.
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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.