ReviewTrends in pharmacological sciences2023
Non-canonical Golgi-compartmentalized Gβγ signaling: mechanisms, functions, and therapeutic targets.
Review in Trends in pharmacological sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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.
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Who cites it
7 citing papers in PubMed.
- MTX-induced gastrointestinal reactions in RA: Prevotella enrichment, gut dysbiosis, and PI3K/Akt/Ras/AMPK pathways.Clinical rheumatology · 2025Article
- A visual cortical-lateral posterior thalamic nucleus circuit regulates depressive-like behaviors in male mice.Nature communications · 2025Article
- The ufmylation cascade controls COPII recruitment, anterograde transport, and sorting of nascent GPCRs at ER.Science advances · 2024Article
- Segregation of nascent GPCRs in the ER-to-Golgi transport by CCHCR1 via direct interaction.Journal of cell science · 2024Article
- The role of Golgi complex proteins in cell division and consequences of their dysregulation.Frontiers in cell and developmental biology · 2024Review
- Article
- Gβγ signaling regulates microtubule-dependent control of Golgi integrity.Cellular signalling · 2023Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
G protein Gβγ subunits are key mediators of G protein-coupled receptor (GPCR) signaling under physiological and pathological conditions; their inhibitors have been tested for the treatment of human disease. Conventional wisdom is that the Gβγ complex is activated and subsequently exerts its functions at the plasma membrane (PM). Recent studies have revealed non-canonical activation of Gβγ at intracellular organelles, where the Golgi apparatus is a major locale, via translocation or local activation. Golgi-localized Gβγ activates specific signaling cascades and regulates fundamental cell processes such as membrane trafficking, proliferation, and migration. More recent studies have shown that inhibiting Golgi-compartmentalized Gβγ signaling attenuates cardiomyocyte hypertrophy and prostate tumorigenesis, indicating new therapeutic targets. We review novel activation mechanisms and non-canonical functions of Gβγ at the Golgi, and discuss potential therapeutic interventions by targeting Golgi-biased Gβγ-directed signaling.
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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.