ArticleThe Journal of biological chemistry2010
Regulation of inositol 1,4,5-trisphosphate receptors by cAMP independent of cAMP-dependent protein kinase.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 50 citations in OpenAlex.
- Glucose Control in Severely Burned Patients Using Metformin: An Interim Safety and Efficacy Analysis of a Phase II Randomized Controlled Trial.Annals of surgery · 2016Trial
- Enhancement of a nuclear factor of activated T cells (NFAT) reporter for the study of G protein-coupled receptors.Communications biology · 2026Article
- A molecular mechanism to diversify CaNature communications · 2024Article
- Dopamine, norepinephrine, and vasopressin accelerate particle transport velocity in murine tracheal epithelium via substance-specific receptor pathways: dependency on intra- and extracellular CaFrontiers in pharmacology · 2024Article
- Article
- Glucagon's Metabolic Action in Health and Disease.Comprehensive Physiology · 2021Article
- Cross-Talk Between the Adenylyl Cyclase/cAMP Pathway and CaReviews of physiology, biochemistry and pharmacology · 2021Review
- The Ion Channel and GPCR Toolkit of Brain Capillary Pericytes.Frontiers in cellular neuroscience · 2020Review
- Determining the Roles of Inositol Trisphosphate Receptors in Neurodegeneration: Interdisciplinary Perspectives on a Complex Topic.Molecular neurobiology · 2017Review
- Regulation of IPCell calcium · 2017Review
- Cyclic AMP Recruits a Discrete Intracellular CaCell reports · 2017Article
- Emergence of ion channel modal gating from independent subunit kinetics.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Differential Dopamine Regulation of Ca(2+) Signaling and Its Timing Dependence in the Nucleus Accumbens.Cell reports · 2016Article
- UTP activates small-conductance Ca2+-activated K+ channels in murine detrusor PDGFRα+ cells.American journal of physiology. Renal physiology · 2015Article
- The type 2 inositol 1,4,5-trisphosphate receptor, emerging functions for an intriguing Ca²⁺-release channel.Biochimica et biophysica acta · 2015Review
- Regulation of calcium clock-mediated pacemaking by inositol-1,4,5-trisphosphate receptors in mouse sinoatrial nodal cells.The Journal of physiology · 2015Article
- Sustained signalling by PTH modulates IP3 accumulation and IP3 receptors through cyclic AMP junctions.Journal of cell science · 2015Article
- Molecular approaches for manipulating astrocytic signaling in vivo.Frontiers in cellular neuroscience · 2015Review
- Calcium release-activated calcium (CRAC) channels mediate the β(2)-adrenergic regulation of Na,K-ATPase.FEBS letters · 2014Article
- Interactions of antagonists with subtypes of inositol 1,4,5-trisphosphate (IP3) receptor.British journal of pharmacology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
In HEK cells stably expressing type 1 receptors for parathyroid hormone (PTH), PTH causes a sensitization of inositol 1,4,5-trisphosphate receptors (IP(3)R) to IP(3) that is entirely mediated by cAMP and requires cAMP to pass directly from type 6 adenylyl cyclase (AC6) to IP(3)R2. Using DT40 cells expressing single subtypes of mammalian IP(3)R, we demonstrate that high concentrations of cAMP similarly sensitize all IP(3)R isoforms to IP(3) by a mechanism that does not require cAMP-dependent protein kinase (PKA). IP(3) binding to IP(3)R2 is unaffected by cAMP, and sensitization is not mediated by the site through which ATP potentiates responses to IP(3). In single channel recordings from excised nuclear patches of cells expressing IP(3)R2, cAMP alone had no effect, but it increased the open probability of IP(3)R2 activated by a submaximal concentration of IP(3) alone or in combination with a maximally effective concentration of ATP. These results establish that cAMP itself increases the sensitivity of all IP(3)R subtypes to IP(3). For IP(3)R2, this sensitization results from cAMP binding to a novel site that increases the efficacy of IP(3). Using stably expressed short hairpin RNA to reduce expression of the G-protein, G alpha(s), we demonstrate that attenuation of AC activity by loss of G alpha(s) more substantially reduces sensitization of IP(3)R by PTH than does comparable direct inhibition of AC. This suggests that G alpha(s) may also specifically associate with each AC x IP(3)R complex. We conclude that all three subtypes of IP(3)R are regulated by cAMP independent of PKA. In HEK cells, where IP(3)R2 selectively associates with AC6, G alpha(s) also associates with the AC x IP(3)R signaling junction.
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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.