ArticleThe Journal of cell biology2005
Junctional membrane inositol 1,4,5-trisphosphate receptor complex coordinates sensitization of the silent EGF-induced Ca2+ signaling.
Article in The Journal of cell biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Altered glucose metabolism and its association with carbonic anhydrase 8 in Machado-Joseph Disease.Metabolic brain disease · 2022Article
- Short DNA/RNA heteroduplex oligonucleotide interacting proteins are key regulators of target gene silencing.Nucleic acids research · 2021Article
- Structural Characterization of Carbonic Anhydrase VIII and Effects of Missense Single Nucleotide Variations to Protein Structure and Function.International journal of molecular sciences · 2020Article
- Inositol 1,4,5-trisphosphate receptors and their protein partners as signalling hubs.The Journal of physiology · 2016Review
- Examining the role of mitochondria in Ca²⁺ signaling in native vascular smooth muscle.Microcirculation (New York, N.Y. : 1994) · 2013Review
- Microdomains of muscarinic acetylcholine and Ins(1,4,5)P₃ receptors create 'Ins(1,4,5)P₃ junctions' and sites of Ca²+ wave initiation in smooth muscle.Journal of cell science · 2012Article
- Inositol 1, 4, 5-trisphosphate receptor interacts with the SNARE domain of syntaxin 1B.The journal of physiological sciences : JPS · 2011Article
- Regulation of inositol 1,4,5-trisphosphate-induced Ca2+ release by reversible phosphorylation and dephosphorylation.Biochimica et biophysica acta · 2009Review
- CA8 mutations cause a novel syndrome characterized by ataxia and mild mental retardation with predisposition to quadrupedal gait.PLoS genetics · 2009Article
- Effects of carbonic anhydrase VIII deficiency on cerebellar gene expression profiles in the wdl mouse.Neuroscience letters · 2007Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca(2+) is a highly versatile intracellular signal that regulates many different cellular processes, and cells have developed mechanisms to have exquisite control over Ca(2+) signaling. Epidermal growth factor (EGF), which fails to mobilize intracellular Ca(2+) when administrated alone, becomes capable of evoking [Ca(2+)](i) increase and exocytosis after bradykinin (BK) stimulation in chromaffin cells. Here, we provide evidence that this sensitization process is coordinated by a macromolecular signaling complex comprised of inositol 1,4,5-trisphosphate receptor type I (IP(3)R1), cAMP-dependent protein kinase (PKA), EGF receptor (EGFR), and an A-kinase anchoring protein, yotiao. The IP(3)R complex functions as a focal point to promote Ca(2+) release in two ways: (1) it facilitates PKA-dependent phosphorylation of IP(3)R1 in response to BK-induced elevation of cAMP, and (2) it couples the plasmalemmal EGFR with IP(3)R1 at the Ca(2+) store located juxtaposed to the plasma membrane. Our study illustrates how the junctional membrane IP(3)R complex connects different signaling pathways to define the fidelity and specificity of Ca(2+) signaling.
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Registered trials
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