ArticleJournal of the Endocrine Society2018
Real-Time Signaling Assays Demonstrate Somatostatin Agonist Bias for Ion Channel Regulation in Somatotroph Tumor Cells.
Article in Journal of the Endocrine Society, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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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.
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Who cites it
1 citing paper in PubMed, 2 citations in OpenAlex.
- Diverse paths for chemoreception in ciliated neurons contacting the cerebrospinal fluid in the spinal cord.bioRxiv : the preprint server for biology · 2026Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
Acromegaly is a neuroendocrine disorder caused by excess secretion of GH by somatotroph tumor cells. It is often treated with somatostatin receptor (SSTR) 2 agonists, which suppress GH secretion. SOM230 is a somatostatin analogue that targets multiple SSTRs and was recently approved for patients with treatment-resistant acromegaly. Previous reports indicate that SOM230 may function as a biased agonist, suggesting that its ability to selectively activate SSTR-dependent signaling events may contribute to its therapeutic efficacy. To better understand how SOM230 modulates Sstr2A function, which is the most commonly expressed SSTR in somatotrophs, we used real-time assays to study SOM230-dependent signaling in rat pituitary tumor cells. We observed that SOM230 suppressed cAMP production in a G
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