ArticleScientific reports2019
A Differential Hypofunctionality of Gαi Proteins Occurs in Adolescent Idiopathic Scoliosis and Correlates with the Risk of Disease Progression.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Loss of Tyrosine Phosphatase Mu Promotes Scoliosis Progression Through Osteopontin-α5β1 Integrin Signaling and PIPK1γ90 Activity.International journal of molecular sciences · 2025Article
- Association between theGenes · 2024Article
- The Role of Muscle Biomarkers in Adolescent Idiopathic Scoliosis.Journal of clinical medicine · 2023Review
- Circulatory Adipokines and Incretins in Adolescent Idiopathic Scoliosis: A Pilot Study.Children (Basel, Switzerland) · 2022Article
- Patient outcomes in idiopathic scoliosis are associated with biological endophenotypes: 2020 SOSORT award winner.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2021Article
- Bone-to-Brain: A Round Trip in the Adaptation to Mechanical Stimuli.Frontiers in physiology · 2021Review
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 6 countries.
Funding
Abstract
Adolescent idiopathic scoliosis is the most prevalent spine deformity and the molecular mechanisms underlying its pathophysiology remain poorly understood. We have previously found a differential impairment of melatonin receptor signaling in AIS osteoblasts allowing the classification of patients into three biological endophenotypes or functional groups (FG1, FG2 and FG3). Here, we provide evidence that the defect characterizing each endophenotype lies at the level of Gαi proteins leading to a systemic and generalized differential impairment of Gi-coupled receptor signaling. The three Gαi isoforms exhibited a selective serine phosphorylation patterns for each AIS endophenotype resulting in a differential reduction in Gαi protein activity as determined by cellular dielectric spectroscopy and small interfering RNA methods. We found that one endophenotype (FG2) with phosphorylated Gαi
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Registered trials
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