ReviewCell calcium
Molecular mechanisms of pituitary endocrine cell calcium handling.
Review in Cell calcium. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed.
- CaNeurochemical research · 2026Article
- Endocrine Disorders of Calcium Signaling in Children: Neuroendocrine Crosstalk and Clinical Implications.Cells · 2026Review
- Noise-Induced Hearing Loss Enhances CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Distribution and calcium signaling function of somatostatin receptor subtypes in rat pituitary.Cell calcium · 2024Article
- Identification of calcium metabolism related score associated with the poor outcome in papillary thyroid carcinoma.Frontiers in oncology · 2023Article
- PI(4,5)P2-dependent and -independent roles of PI4P in the control of hormone secretion by pituitary cells.Frontiers in endocrinology · 2023Review
- Expression and Role of Thyrotropin Receptors in Proopiomelanocortin-Producing Pituitary Cells.Thyroid : official journal of the American Thyroid Association · 2021Article
- Long extensions with varicosity-like structures in gonadotrope Lh cells facilitate clustering in medaka pituitary culture.PloS one · 2021Article
- Imaging of Endoplasmic Reticulum CaFrontiers in endocrinology · 2020Article
- A computational model for gonadotropin releasing cells in the teleost fish medaka.PLoS computational biology · 2019Article
- GnRH-A Key Regulator of FSH.Endocrinology · 2019Review
- Real-Time Signaling Assays Demonstrate Somatostatin Agonist Bias for Ion Channel Regulation in Somatotroph Tumor Cells.Journal of the Endocrine Society · 2018Article
- Common and diverse elements of ion channels and receptors underlying electrical activity in endocrine pituitary cells.Molecular and cellular endocrinology · 2018Review
- Regulation of reproduction via tight control of gonadotropin hormone levels.Molecular and cellular endocrinology · 2018Review
- Mathematical modeling of gonadotropin-releasing hormone signaling.Molecular and cellular endocrinology · 2017Review
- Ion Channels of Pituitary Gonadotrophs and Their Roles in Signaling and Secretion.Frontiers in endocrinology · 2017Review
- Gap junction proteins in the blood-brain barrier control nutrient-dependent reactivation of Drosophila neural stem cells.Developmental cell · 2014Article
- GnRH-Induced Ca(2+) Signaling Patterns and Gonadotropin Secretion in Pituitary Gonadotrophs. Functional Adaptations to Both Ordinary and Extraordinary Physiological Demands.Frontiers in endocrinology · 2013Review
- Dependence of the excitability of pituitary cells on cyclic nucleotides.Journal of neuroendocrinology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
Endocrine pituitary cells express numerous voltage-gated Na(+), Ca(2+), K(+), and Cl(-) channels and several ligand-gated channels, and they fire action potentials spontaneously. Depending on the cell type, this electrical activity can generate localized or global Ca(2+) signals, the latter reaching the threshold for stimulus-secretion coupling. These cells also express numerous G-protein-coupled receptors, which can stimulate or silence electrical activity and Ca(2+) influx through voltage-gated Ca(2+) channels and hormone release. Receptors positively coupled to the adenylyl cyclase signaling pathway stimulate electrical activity with cAMP, which activates hyperpolarization-activated cyclic nucleotide-regulated channels directly, or by cAMP-dependent kinase-mediated phosphorylation of K(+), Na(+), Ca(2+), and/or non-selective cation-conducting channels. Receptors that are negatively coupled to adenylyl cyclase signaling pathways inhibit spontaneous electrical activity and accompanied Ca(2+) transients predominantly through the activation of inwardly rectifying K(+) channels and the inhibition of voltage-gated Ca(2+) channels. The Ca(2+)-mobilizing receptors activate inositol trisphosphate-gated Ca(2+) channels in the endoplasmic reticulum, leading to Ca(2+) release in an oscillatory or non-oscillatory manner, depending on the cell type. This Ca(2+) release causes a cell type-specific modulation of electrical activity and intracellular Ca(2+) handling.
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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.