ArticleProceedings of the National Academy of Sciences of the United States of America1993
Gi2 and protein kinase C are required for thyrotropin-releasing hormone-induced stimulation of voltage-dependent Ca2+ channels in rat pituitary GH3 cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- Association of genetic variants in GNβ3 with functional dyspepsia: a meta-analysis.Digestive diseases and sciences · 2014Pooled it
- Biochemical and physiological insights into TRH receptor-mediated signaling.Frontiers in cell and developmental biology · 2022Review
- Ion channels and signaling in the pituitary gland.Endocrine reviews · 2010Review
- Coupling specificity of NOP opioid receptors to pertussis-toxin-sensitive Galpha proteins in adult rat stellate ganglion neurons using small interference RNA.Journal of neurophysiology · 2008Article
- Homozygous 825T allele of the GNB3 protein influences the susceptibility of Japanese to dyspepsia.Digestive diseases and sciences · 2008Article
- Synaptic control of motoneuronal excitability.Physiological reviews · 2000Review
- Receptor-activated Ca2+ inflow in animal cells: a variety of pathways tailored to meet different intracellular Ca2+ signalling requirements.The Biochemical journal · 1999Review
- Multifactorial modulation of TRH metabolism.Cellular and molecular neurobiology · 1998Review
- Evidence that a low-molecular-mass GTP-binding protein is required for store-activated Ca2+ inflow in hepatocytes.The Biochemical journal · 1997Article
- Signalling functions and biochemical properties of pertussis toxin-resistant G-proteins.The Biochemical journal · 1997Review
- Distinct roles for two G protein alpha subunits in fungal virulence, morphology, and reproduction revealed by targeted gene disruption.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Characterization of the G protein coupling of SRIF and beta-adrenergic receptors to the maxi KCa channel in insulin-secreting cells.The Journal of membrane biology · 1995Article
- Subunit composition of G(o) proteins functionally coupling galanin receptors to voltage-gated calcium channels.The EMBO journal · 1995Article
- Comparison of the signalling properties of the long and short isoforms of the rat thyrotropin-releasing-hormone receptor following expression in rat 1 fibroblasts.The Biochemical journal · 1995Article
- A Gi1-2-protein is required for alpha 2A-adrenoceptor-induced stimulation of voltage-dependent Ca2+ channels in rat portal vein myocytes.Pflugers Archiv : European journal of physiology · 1995Article
- Stimulation of single L-type calcium channels in rat pituitary GH3 cells by thyrotropin-releasing hormone.The EMBO journal · 1995Article
- Receptors and G proteins as primary components of transmembrane signal transduction. Part 2. G proteins: structure and function.Journal of molecular medicine (Berlin, Germany) · 1995Review
- Evidence from studies with hepatocyte suspensions that store-operated Ca2+ inflow requires a pertussis toxin-sensitive trimeric G-protein.The Biochemical journal · 1994Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In rat pituitary GH3 cells, thyrotropin-releasing hormone (TRH) and other secretion-stimulating hormones trigger an increase in the cytosolic Ca2+ concentration by two mechanisms. Ca2+ is released from intracellular stores in response to inositol 1,4,5-trisphosphate and can enter the cell through voltage-dependent L-type Ca2+ channels. Stimulation of these channels is sensitive to pertussis toxin, indicating that a pertussis toxin-sensitive heterotrimeric guanine nucleotide-binding regulatory protein (G protein) is involved in functional coupling of the receptor to the Ca2+ channel. We identified the G protein involved in the stimulatory effect of TRH on the Ca2+ channel by type-selective suppression of G-protein synthesis. Antisense oligonucleotides were microinjected into GH3 cell nuclei, and 48 h after injection the TRH effect was tested. Whereas antisense oligonucleotides hybridizing to the mRNA of G(o) or Gi1 alpha-subunit sequences did not affect stimulation by TRH, oligonucleotides suppressing the expression of the Gi2 alpha subunit abolished this effect, and oligonucleotides directed against the mRNA of the Gi3 alpha subunit had less effect. The requirement of a concurrent inositol phospholipid degradation and subsequent protein kinase C (PKC) activation for the TRH effect on Ca(2+)-channel activity was demonstrated by inhibitory effects of antisense oligonucleotides directed against Gq/G11/Gz alpha-subunit sequences and treatment of GH3 cells with PKC inhibitors, respectively. Our results suggest that TRH elevates the cytosolic Ca2+ concentration in GH3 cells transiently via Ca2+ release from internal stores, followed by a phase of sustained Ca2+ influx through voltage-dependent Ca2+ channels stimulated by the concerted action of Gi2 (and Gi3) plus PKC.
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